Binding of bacteria to HEp-2 cells infected with influenza A virus
Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ahmer, Omar R [verfasserIn] Raza, Muhammed W [verfasserIn] Ogilvie, Marie M [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|
| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1999 |
|---|
| Schlagwörter: |
|---|
| Umfang: |
Online-Ressource |
|---|
| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
|---|---|
| Übergeordnetes Werk: |
In: FEMS immunology and medical microbiology - Federation of European Microbiological Societies ; GKD-ID: 114439X, Oxford [u.a.] : Wiley-Blackwell, 1993, 23(1999), 4, Seite 0 |
| Übergeordnetes Werk: |
volume:23 ; year:1999 ; number:4 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1111/j.1574-695X.1999.tb01255.x |
|---|
| Katalog-ID: |
NLEJ242931529 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ242931529 | ||
| 003 | DE-627 | ||
| 005 | 20230506111302.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 120427s1999 xx |||||o 00| ||und c | ||
| 024 | 7 | |a 10.1111/j.1574-695X.1999.tb01255.x |2 doi | |
| 035 | |a (DE-627)NLEJ242931529 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 100 | 1 | |a Ahmer, Omar R |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Binding of bacteria to HEp-2 cells infected with influenza A virus |
| 264 | 1 | |a Oxford, UK |b Blackwell Publishing Ltd |c 1999 | |
| 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 Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). | ||
| 533 | |d 2006 |f Blackwell Publishing Journal Backfiles 1879-2005 |7 |2006|||||||||| | ||
| 650 | 4 | |a Influenza A virus | |
| 700 | 1 | |a Raza, Muhammed W |e verfasserin |4 aut | |
| 700 | 1 | |a Ogilvie, Marie M |e verfasserin |4 aut | |
| 700 | 1 | |a Weir, Donald M |4 oth | |
| 700 | 1 | |a Blackwell, C.Caroline |4 oth | |
| 773 | 0 | 8 | |i In |a Federation of European Microbiological Societies ; GKD-ID: 114439X |t FEMS immunology and medical microbiology |d Oxford [u.a.] : Wiley-Blackwell, 1993 |g 23(1999), 4, Seite 0 |h Online-Ressource |w (DE-627)NLEJ243926014 |w (DE-600)1500464-8 |x 1574-695X |7 nnns |
| 773 | 1 | 8 | |g volume:23 |g year:1999 |g number:4 |g pages:0 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.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 23 |j 1999 |e 4 |h 0 | ||
| author_variant |
o r a or ora m w r mw mwr m m o mm mmo |
|---|---|
| matchkey_str |
article:1574695X:1999----::idnobceithpclsnetdi |
| hierarchy_sort_str |
1999 |
| publishDate |
1999 |
| allfields |
10.1111/j.1574-695X.1999.tb01255.x doi (DE-627)NLEJ242931529 DE-627 ger DE-627 rakwb Ahmer, Omar R verfasserin aut Binding of bacteria to HEp-2 cells infected with influenza A virus Oxford, UK Blackwell Publishing Ltd 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Influenza A virus Raza, Muhammed W verfasserin aut Ogilvie, Marie M verfasserin aut Weir, Donald M oth Blackwell, C.Caroline oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 23(1999), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:23 year:1999 number:4 pages:0 http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1999 4 0 |
| spelling |
10.1111/j.1574-695X.1999.tb01255.x doi (DE-627)NLEJ242931529 DE-627 ger DE-627 rakwb Ahmer, Omar R verfasserin aut Binding of bacteria to HEp-2 cells infected with influenza A virus Oxford, UK Blackwell Publishing Ltd 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Influenza A virus Raza, Muhammed W verfasserin aut Ogilvie, Marie M verfasserin aut Weir, Donald M oth Blackwell, C.Caroline oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 23(1999), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:23 year:1999 number:4 pages:0 http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1999 4 0 |
| allfields_unstemmed |
10.1111/j.1574-695X.1999.tb01255.x doi (DE-627)NLEJ242931529 DE-627 ger DE-627 rakwb Ahmer, Omar R verfasserin aut Binding of bacteria to HEp-2 cells infected with influenza A virus Oxford, UK Blackwell Publishing Ltd 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Influenza A virus Raza, Muhammed W verfasserin aut Ogilvie, Marie M verfasserin aut Weir, Donald M oth Blackwell, C.Caroline oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 23(1999), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:23 year:1999 number:4 pages:0 http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1999 4 0 |
| allfieldsGer |
10.1111/j.1574-695X.1999.tb01255.x doi (DE-627)NLEJ242931529 DE-627 ger DE-627 rakwb Ahmer, Omar R verfasserin aut Binding of bacteria to HEp-2 cells infected with influenza A virus Oxford, UK Blackwell Publishing Ltd 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Influenza A virus Raza, Muhammed W verfasserin aut Ogilvie, Marie M verfasserin aut Weir, Donald M oth Blackwell, C.Caroline oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 23(1999), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:23 year:1999 number:4 pages:0 http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1999 4 0 |
| allfieldsSound |
10.1111/j.1574-695X.1999.tb01255.x doi (DE-627)NLEJ242931529 DE-627 ger DE-627 rakwb Ahmer, Omar R verfasserin aut Binding of bacteria to HEp-2 cells infected with influenza A virus Oxford, UK Blackwell Publishing Ltd 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Influenza A virus Raza, Muhammed W verfasserin aut Ogilvie, Marie M verfasserin aut Weir, Donald M oth Blackwell, C.Caroline oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 23(1999), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:23 year:1999 number:4 pages:0 http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1999 4 0 |
| source |
In FEMS immunology and medical microbiology 23(1999), 4, Seite 0 volume:23 year:1999 number:4 pages:0 |
| sourceStr |
In FEMS immunology and medical microbiology 23(1999), 4, Seite 0 volume:23 year:1999 number:4 pages:0 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
Influenza A virus |
| isfreeaccess_bool |
false |
| container_title |
FEMS immunology and medical microbiology |
| authorswithroles_txt_mv |
Ahmer, Omar R @@aut@@ Raza, Muhammed W @@aut@@ Ogilvie, Marie M @@aut@@ Weir, Donald M @@oth@@ Blackwell, C.Caroline @@oth@@ |
| publishDateDaySort_date |
1999-01-01T00:00:00Z |
| hierarchy_top_id |
NLEJ243926014 |
| id |
NLEJ242931529 |
| 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">NLEJ242931529</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506111302.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s1999 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1574-695X.1999.tb01255.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242931529</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="100" ind1="1" ind2=" "><subfield code="a">Ahmer, Omar R</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Binding of bacteria to HEp-2 cells infected with influenza A virus</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Publishing Ltd</subfield><subfield code="c">1999</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">Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05).</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2006</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2006||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Influenza A virus</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Raza, Muhammed W</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ogilvie, Marie M</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Weir, Donald M</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Blackwell, C.Caroline</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="a">Federation of European Microbiological Societies ; GKD-ID: 114439X</subfield><subfield code="t">FEMS immunology and medical microbiology</subfield><subfield code="d">Oxford [u.a.] : Wiley-Blackwell, 1993</subfield><subfield code="g">23(1999), 4, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926014</subfield><subfield code="w">(DE-600)1500464-8</subfield><subfield code="x">1574-695X</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:23</subfield><subfield code="g">year:1999</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.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">23</subfield><subfield code="j">1999</subfield><subfield code="e">4</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| series2 |
Blackwell Publishing Journal Backfiles 1879-2005 |
| author |
Ahmer, Omar R |
| spellingShingle |
Ahmer, Omar R misc Influenza A virus Binding of bacteria to HEp-2 cells infected with influenza A virus |
| authorStr |
Ahmer, Omar R |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ243926014 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut aut |
| collection |
NL |
| publishPlace |
Oxford, UK |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1574-695X |
| topic_title |
Binding of bacteria to HEp-2 cells infected with influenza A virus Influenza A virus |
| publisher |
Blackwell Publishing Ltd |
| publisherStr |
Blackwell Publishing Ltd |
| topic |
misc Influenza A virus |
| topic_unstemmed |
misc Influenza A virus |
| topic_browse |
misc Influenza A virus |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
d m w dm dmw c b cb |
| hierarchy_parent_title |
FEMS immunology and medical microbiology |
| hierarchy_parent_id |
NLEJ243926014 |
| hierarchy_top_title |
FEMS immunology and medical microbiology |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ243926014 (DE-600)1500464-8 |
| title |
Binding of bacteria to HEp-2 cells infected with influenza A virus |
| ctrlnum |
(DE-627)NLEJ242931529 |
| title_full |
Binding of bacteria to HEp-2 cells infected with influenza A virus |
| author_sort |
Ahmer, Omar R |
| journal |
FEMS immunology and medical microbiology |
| journalStr |
FEMS immunology and medical microbiology |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
1999 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Ahmer, Omar R Raza, Muhammed W Ogilvie, Marie M |
| container_volume |
23 |
| physical |
Online-Ressource |
| format_se |
Elektronische Aufsätze |
| author-letter |
Ahmer, Omar R |
| doi_str_mv |
10.1111/j.1574-695X.1999.tb01255.x |
| author2-role |
verfasserin |
| title_sort |
binding of bacteria to hep-2 cells infected with influenza a virus |
| title_auth |
Binding of bacteria to HEp-2 cells infected with influenza A virus |
| abstract |
Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). |
| abstractGer |
Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). |
| abstract_unstemmed |
Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05). |
| collection_details |
GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE |
| container_issue |
4 |
| title_short |
Binding of bacteria to HEp-2 cells infected with influenza A virus |
| url |
http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.x |
| remote_bool |
true |
| author2 |
Raza, Muhammed W Ogilvie, Marie M Weir, Donald M Blackwell, C.Caroline |
| author2Str |
Raza, Muhammed W Ogilvie, Marie M Weir, Donald M Blackwell, C.Caroline |
| ppnlink |
NLEJ243926014 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth |
| doi_str |
10.1111/j.1574-695X.1999.tb01255.x |
| up_date |
2024-07-06T03:43:08.375Z |
| _version_ |
1803799639754801152 |
| 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">NLEJ242931529</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506111302.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s1999 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1574-695X.1999.tb01255.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242931529</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="100" ind1="1" ind2=" "><subfield code="a">Ahmer, Omar R</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Binding of bacteria to HEp-2 cells infected with influenza A virus</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Publishing Ltd</subfield><subfield code="c">1999</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">Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P<0.05) and CD18 (P<0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P<0.001) and CD18 (P<0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P<0.01) and CD18 (P<0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P<0.05).</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2006</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2006||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Influenza A virus</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Raza, Muhammed W</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ogilvie, Marie M</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Weir, Donald M</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Blackwell, C.Caroline</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="a">Federation of European Microbiological Societies ; GKD-ID: 114439X</subfield><subfield code="t">FEMS immunology and medical microbiology</subfield><subfield code="d">Oxford [u.a.] : Wiley-Blackwell, 1993</subfield><subfield code="g">23(1999), 4, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926014</subfield><subfield code="w">(DE-600)1500464-8</subfield><subfield code="x">1574-695X</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:23</subfield><subfield code="g">year:1999</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1111/j.1574-695X.1999.tb01255.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">23</subfield><subfield code="j">1999</subfield><subfield code="e">4</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.4010878 |