Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model
Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
|---|
| Format: |
E-Artikel |
|---|
| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2002 |
|---|
| Schlagwörter: |
|---|
| Umfang: |
Online-Ressource |
|---|
| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
|---|---|
| Übergeordnetes Werk: |
In: Clinical & experimental allergy - Oxford : Blackwell Science, 1989, 32(2002), 6, Seite 0 |
| Übergeordnetes Werk: |
volume:32 ; year:2002 ; number:6 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1046/j.1365-2222.2002.01362.x |
|---|
| Katalog-ID: |
NLEJ242609945 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ242609945 | ||
| 003 | DE-627 | ||
| 005 | 20210707161606.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 120427s2002 xx |||||o 00| ||und c | ||
| 024 | 7 | |a 10.1046/j.1365-2222.2002.01362.x |2 doi | |
| 035 | |a (DE-627)NLEJ242609945 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 245 | 1 | 0 | |a Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| 264 | 1 | |a Oxford, UK |b Blackwell Science Ltd |c 2002 | |
| 300 | |a Online-Ressource | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. | ||
| 533 | |d 2002 |f Blackwell Publishing Journal Backfiles 1879-2005 |7 |2002|||||||||| | ||
| 650 | 4 | |a bronchial epithelial cells | |
| 700 | 1 | |a Kato, Y. |4 oth | |
| 700 | 1 | |a Fujisawa, T. |4 oth | |
| 700 | 1 | |a Shibano, M. |4 oth | |
| 700 | 1 | |a Saito, T. |4 oth | |
| 700 | 1 | |a Gatto, W. |4 oth | |
| 700 | 1 | |a Kamiya, H. |4 oth | |
| 700 | 1 | |a Hirai, K. |4 oth | |
| 700 | 1 | |a Sumida, M. |4 oth | |
| 700 | 1 | |a Yoshie, O. |4 oth | |
| 773 | 0 | 8 | |i In |t Clinical & experimental allergy |d Oxford : Blackwell Science, 1989 |g 32(2002), 6, Seite 0 |h Online-Ressource |w (DE-627)NLEJ243926391 |w (DE-600)2004469-0 |x 1365-2222 |7 nnns |
| 773 | 1 | 8 | |g volume:32 |g year:2002 |g number:6 |g pages:0 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x |q text/html |x Verlag |z Deutschlandweit zugänglich |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-DJB | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 32 |j 2002 |e 6 |h 0 | ||
| matchkey_str |
article:13652222:2002----::iwypteilelpooernmgainfoiohliaetrei |
|---|---|
| hierarchy_sort_str |
2002 |
| publishDate |
2002 |
| allfields |
10.1046/j.1365-2222.2002.01362.x doi (DE-627)NLEJ242609945 DE-627 ger DE-627 rakwb Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| bronchial epithelial cells Kato, Y. oth Fujisawa, T. oth Shibano, M. oth Saito, T. oth Gatto, W. oth Kamiya, H. oth Hirai, K. oth Sumida, M. oth Yoshie, O. oth In Clinical & experimental allergy Oxford : Blackwell Science, 1989 32(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926391 (DE-600)2004469-0 1365-2222 nnns volume:32 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 32 2002 6 0 |
| spelling |
10.1046/j.1365-2222.2002.01362.x doi (DE-627)NLEJ242609945 DE-627 ger DE-627 rakwb Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| bronchial epithelial cells Kato, Y. oth Fujisawa, T. oth Shibano, M. oth Saito, T. oth Gatto, W. oth Kamiya, H. oth Hirai, K. oth Sumida, M. oth Yoshie, O. oth In Clinical & experimental allergy Oxford : Blackwell Science, 1989 32(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926391 (DE-600)2004469-0 1365-2222 nnns volume:32 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 32 2002 6 0 |
| allfields_unstemmed |
10.1046/j.1365-2222.2002.01362.x doi (DE-627)NLEJ242609945 DE-627 ger DE-627 rakwb Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| bronchial epithelial cells Kato, Y. oth Fujisawa, T. oth Shibano, M. oth Saito, T. oth Gatto, W. oth Kamiya, H. oth Hirai, K. oth Sumida, M. oth Yoshie, O. oth In Clinical & experimental allergy Oxford : Blackwell Science, 1989 32(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926391 (DE-600)2004469-0 1365-2222 nnns volume:32 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 32 2002 6 0 |
| allfieldsGer |
10.1046/j.1365-2222.2002.01362.x doi (DE-627)NLEJ242609945 DE-627 ger DE-627 rakwb Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| bronchial epithelial cells Kato, Y. oth Fujisawa, T. oth Shibano, M. oth Saito, T. oth Gatto, W. oth Kamiya, H. oth Hirai, K. oth Sumida, M. oth Yoshie, O. oth In Clinical & experimental allergy Oxford : Blackwell Science, 1989 32(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926391 (DE-600)2004469-0 1365-2222 nnns volume:32 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 32 2002 6 0 |
| allfieldsSound |
10.1046/j.1365-2222.2002.01362.x doi (DE-627)NLEJ242609945 DE-627 ger DE-627 rakwb Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| bronchial epithelial cells Kato, Y. oth Fujisawa, T. oth Shibano, M. oth Saito, T. oth Gatto, W. oth Kamiya, H. oth Hirai, K. oth Sumida, M. oth Yoshie, O. oth In Clinical & experimental allergy Oxford : Blackwell Science, 1989 32(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926391 (DE-600)2004469-0 1365-2222 nnns volume:32 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 32 2002 6 0 |
| source |
In Clinical & experimental allergy 32(2002), 6, Seite 0 volume:32 year:2002 number:6 pages:0 |
| sourceStr |
In Clinical & experimental allergy 32(2002), 6, Seite 0 volume:32 year:2002 number:6 pages:0 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
bronchial epithelial cells |
| isfreeaccess_bool |
false |
| container_title |
Clinical & experimental allergy |
| authorswithroles_txt_mv |
Kato, Y. @@oth@@ Fujisawa, T. @@oth@@ Shibano, M. @@oth@@ Saito, T. @@oth@@ Gatto, W. @@oth@@ Kamiya, H. @@oth@@ Hirai, K. @@oth@@ Sumida, M. @@oth@@ Yoshie, O. @@oth@@ |
| publishDateDaySort_date |
2002-01-01T00:00:00Z |
| hierarchy_top_id |
NLEJ243926391 |
| id |
NLEJ242609945 |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ242609945</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707161606.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2002 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1365-2222.2002.01362.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242609945</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2002</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2002</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2002||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">bronchial epithelial cells</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kato, Y.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fujisawa, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shibano, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saito, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gatto, W.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kamiya, H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hirai, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sumida, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yoshie, O.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Clinical & experimental allergy</subfield><subfield code="d">Oxford : Blackwell Science, 1989</subfield><subfield code="g">32(2002), 6, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926391</subfield><subfield code="w">(DE-600)2004469-0</subfield><subfield code="x">1365-2222</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:32</subfield><subfield code="g">year:2002</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">32</subfield><subfield code="j">2002</subfield><subfield code="e">6</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| series2 |
Blackwell Publishing Journal Backfiles 1879-2005 |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ243926391 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| collection |
NL |
| publishPlace |
Oxford, UK |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1365-2222 |
| topic_title |
Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model bronchial epithelial cells |
| publisher |
Blackwell Science Ltd |
| publisherStr |
Blackwell Science Ltd |
| topic |
misc bronchial epithelial cells |
| spellingShingle |
misc bronchial epithelial cells Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| topic_unstemmed |
misc bronchial epithelial cells |
| topic_browse |
misc bronchial epithelial cells |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
y k yk t f tf m s ms t s ts w g wg h k hk k h kh m s ms o y oy |
| hierarchy_parent_title |
Clinical & experimental allergy |
| hierarchy_parent_id |
NLEJ243926391 |
| hierarchy_top_title |
Clinical & experimental allergy |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ243926391 (DE-600)2004469-0 |
| title |
Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| ctrlnum |
(DE-627)NLEJ242609945 |
| title_full |
Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| journal |
Clinical & experimental allergy |
| journalStr |
Clinical & experimental allergy |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
2002 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| container_volume |
32 |
| physical |
Online-Ressource |
| format_se |
Elektronische Aufsätze |
| doi_str_mv |
10.1046/j.1365-2222.2002.01362.x |
| title_sort |
airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| title_auth |
Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| abstract |
Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. |
| abstractGer |
Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. |
| abstract_unstemmed |
Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration. |
| collection_details |
GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE |
| container_issue |
6 |
| title_short |
Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model |
| url |
http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x |
| remote_bool |
true |
| author2 |
Kato, Y. Fujisawa, T. Shibano, M. Saito, T. Gatto, W. Kamiya, H. Hirai, K. Sumida, M. Yoshie, O. |
| author2Str |
Kato, Y. Fujisawa, T. Shibano, M. Saito, T. Gatto, W. Kamiya, H. Hirai, K. Sumida, M. Yoshie, O. |
| ppnlink |
NLEJ243926391 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1046/j.1365-2222.2002.01362.x |
| up_date |
2024-07-06T02:34:49.926Z |
| _version_ |
1803795342218493952 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ242609945</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707161606.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2002 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1365-2222.2002.01362.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242609945</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Airway epithelial cells promote transmigration of eosinophils in a new three-dimensional chemotaxis model</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2002</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Prominent infiltration of eosinophils in airway mucosa is the pathognomonic sign of asthma. The role of airway epithelial cells in eosinophil infiltration, however, has not been fully elucidated.Objective The aim of this study is to develop a new in vitro transmigration system composed of airway epithelial cells and extracellular matrix, and to investigate the role of airway epithelial cells in eosinophil infiltration.Methods A layer of type I collagen gel was formed in Netwell™, and BEAS-2B bronchial epithelial cells were cultured on the gel. Then the wells covered with epithelial monolayer were filled with medium, inverted, and new upper chambers were constructed on the gel side by applying a ring cap. After further incubation with or without exogenous cytokines for 48 h, eosinophils or neutrophils were loaded in upper chambers (the gel side) and cells transmigrated to lower chambers (the epithelial cell side) were counted. Immunohistochemical analyses were also performed.Results While a simple collagen gel hardly promoted eosinophil migration even in the presence of eotaxin or RANTES, significant numbers of eosinophils migrated to lower chambers in the presence of the epithelial cells. Replacement of medium in the lower chamber (the epithelial cell side) with fresh medium, addition of exogenous eotaxin or RANTES in the upper chamber (the gel side), or pre-treatment of eosinophils with anti-CCR3 all inhibited transmigration. We found that the epithelial cells produced and deposited extracellular matrix proteins such as type IV collagen onto the type I collagen gel. Separately, we found that type IV collagen itself was capable of enhancing eotaxin-induced eosinophil migration in a standard chemotaxis assay. Neutrophils also efficiently migrated in the present transmigration system. Pre-treatment of epithelial cells with TNF-α and IL-4 enhanced eosinophil transmigration, while that of neutrophils was enhanced by TNF-α but suppressed by IL-4.Conclusion By utilizing a new in vitro transmigration system mimicking the airway mucosa, we have demonstrated that airway epithelial cells play an essential role in transmigration of eosinophils and that multiple factors such as chemokines, extracellular matrix proteins and exogenous inflammatory cytokines are involved in efficient transmigration.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2002</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2002||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">bronchial epithelial cells</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kato, Y.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fujisawa, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shibano, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saito, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gatto, W.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kamiya, H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hirai, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sumida, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yoshie, O.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Clinical & experimental allergy</subfield><subfield code="d">Oxford : Blackwell Science, 1989</subfield><subfield code="g">32(2002), 6, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926391</subfield><subfield code="w">(DE-600)2004469-0</subfield><subfield code="x">1365-2222</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:32</subfield><subfield code="g">year:2002</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1365-2222.2002.01362.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">32</subfield><subfield code="j">2002</subfield><subfield code="e">6</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.4010057 |