Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency

Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induc...
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Autor*in:	Schmiedl, Andreas [verfasserIn] Wagener, Inga [verfasserIn] Jungen, Meike [verfasserIn] von Hörsten, Stephan [verfasserIn] Stephan, Michael [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Rat Lung development Lipopolysaccharide (LPS) CD26/DPP4 Immune cells

Anmerkung:	© The Author(s) 2021

Übergeordnetes Werk:	Enthalten in: Cell & tissue research - Berlin : Springer, 1924, 386(2021), 3 vom: 04. Okt., Seite 617-636
Übergeordnetes Werk:	volume:386 ; year:2021 ; number:3 ; day:04 ; month:10 ; pages:617-636

Links:	Volltext

DOI / URN:	10.1007/s00441-021-03522-8

Katalog-ID:	SPR045587876

Internformat


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100	1		\|a Schmiedl, Andreas \|e verfasserin \|4 aut
245	1	0	\|a Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
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520			\|a Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition.
650		4	\|a Rat \|7 (dpeaa)DE-He213
650		4	\|a Lung development \|7 (dpeaa)DE-He213
650		4	\|a Lipopolysaccharide (LPS) \|7 (dpeaa)DE-He213
650		4	\|a CD26/DPP4 \|7 (dpeaa)DE-He213
650		4	\|a Immune cells \|7 (dpeaa)DE-He213
700	1		\|a Wagener, Inga \|e verfasserin \|4 aut
700	1		\|a Jungen, Meike \|e verfasserin \|4 aut
700	1		\|a von Hörsten, Stephan \|e verfasserin \|4 aut
700	1		\|a Stephan, Michael \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Cell & tissue research \|d Berlin : Springer, 1924 \|g 386(2021), 3 vom: 04. Okt., Seite 617-636 \|w (DE-627)253390516 \|w (DE-600)1458496-7 \|x 1432-0878 \|7 nnns
773	1	8	\|g volume:386 \|g year:2021 \|g number:3 \|g day:04 \|g month:10 \|g pages:617-636
856	4	0	\|u https://dx.doi.org/10.1007/s00441-021-03522-8 \|z kostenfrei \|3 Volltext
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912			\|a GBV_ILN_70
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_90
912			\|a GBV_ILN_95
912			\|a GBV_ILN_100
912			\|a GBV_ILN_101
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_120
912			\|a GBV_ILN_138
912			\|a GBV_ILN_150
912			\|a GBV_ILN_151
912			\|a GBV_ILN_152
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_171
912			\|a GBV_ILN_187
912			\|a GBV_ILN_213
912			\|a GBV_ILN_224
912			\|a GBV_ILN_230
912			\|a GBV_ILN_250
912			\|a GBV_ILN_267
912			\|a GBV_ILN_281
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_370
912			\|a GBV_ILN_602
912			\|a GBV_ILN_636
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2004
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2007
912			\|a GBV_ILN_2008
912			\|a GBV_ILN_2009
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2025
912			\|a GBV_ILN_2026
912			\|a GBV_ILN_2027
912			\|a GBV_ILN_2031
912			\|a GBV_ILN_2034
912			\|a GBV_ILN_2037
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2039
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2049
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2055
912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
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Indexfelder

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matchkey_str	article:14320878:2021----::ugeeomnadmuettsnecrncpepsrirtusihn
hierarchy_sort_str	2021
bklnumber	42.15
publishDate	2021
allfields	10.1007/s00441-021-03522-8 doi (DE-627)SPR045587876 (SPR)s00441-021-03522-8-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Schmiedl, Andreas verfasserin aut Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213 Wagener, Inga verfasserin aut Jungen, Meike verfasserin aut von Hörsten, Stephan verfasserin aut Stephan, Michael verfasserin aut Enthalten in Cell & tissue research Berlin : Springer, 1924 386(2021), 3 vom: 04. Okt., Seite 617-636 (DE-627)253390516 (DE-600)1458496-7 1432-0878 nnns volume:386 year:2021 number:3 day:04 month:10 pages:617-636 https://dx.doi.org/10.1007/s00441-021-03522-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 386 2021 3 04 10 617-636
spelling	10.1007/s00441-021-03522-8 doi (DE-627)SPR045587876 (SPR)s00441-021-03522-8-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Schmiedl, Andreas verfasserin aut Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213 Wagener, Inga verfasserin aut Jungen, Meike verfasserin aut von Hörsten, Stephan verfasserin aut Stephan, Michael verfasserin aut Enthalten in Cell & tissue research Berlin : Springer, 1924 386(2021), 3 vom: 04. Okt., Seite 617-636 (DE-627)253390516 (DE-600)1458496-7 1432-0878 nnns volume:386 year:2021 number:3 day:04 month:10 pages:617-636 https://dx.doi.org/10.1007/s00441-021-03522-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 386 2021 3 04 10 617-636
allfields_unstemmed	10.1007/s00441-021-03522-8 doi (DE-627)SPR045587876 (SPR)s00441-021-03522-8-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Schmiedl, Andreas verfasserin aut Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213 Wagener, Inga verfasserin aut Jungen, Meike verfasserin aut von Hörsten, Stephan verfasserin aut Stephan, Michael verfasserin aut Enthalten in Cell & tissue research Berlin : Springer, 1924 386(2021), 3 vom: 04. Okt., Seite 617-636 (DE-627)253390516 (DE-600)1458496-7 1432-0878 nnns volume:386 year:2021 number:3 day:04 month:10 pages:617-636 https://dx.doi.org/10.1007/s00441-021-03522-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 386 2021 3 04 10 617-636
allfieldsGer	10.1007/s00441-021-03522-8 doi (DE-627)SPR045587876 (SPR)s00441-021-03522-8-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Schmiedl, Andreas verfasserin aut Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213 Wagener, Inga verfasserin aut Jungen, Meike verfasserin aut von Hörsten, Stephan verfasserin aut Stephan, Michael verfasserin aut Enthalten in Cell & tissue research Berlin : Springer, 1924 386(2021), 3 vom: 04. Okt., Seite 617-636 (DE-627)253390516 (DE-600)1458496-7 1432-0878 nnns volume:386 year:2021 number:3 day:04 month:10 pages:617-636 https://dx.doi.org/10.1007/s00441-021-03522-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 386 2021 3 04 10 617-636
allfieldsSound	10.1007/s00441-021-03522-8 doi (DE-627)SPR045587876 (SPR)s00441-021-03522-8-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Schmiedl, Andreas verfasserin aut Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213 Wagener, Inga verfasserin aut Jungen, Meike verfasserin aut von Hörsten, Stephan verfasserin aut Stephan, Michael verfasserin aut Enthalten in Cell & tissue research Berlin : Springer, 1924 386(2021), 3 vom: 04. Okt., Seite 617-636 (DE-627)253390516 (DE-600)1458496-7 1432-0878 nnns volume:386 year:2021 number:3 day:04 month:10 pages:617-636 https://dx.doi.org/10.1007/s00441-021-03522-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 386 2021 3 04 10 617-636
language	English
source	Enthalten in Cell & tissue research 386(2021), 3 vom: 04. Okt., Seite 617-636 volume:386 year:2021 number:3 day:04 month:10 pages:617-636
sourceStr	Enthalten in Cell & tissue research 386(2021), 3 vom: 04. Okt., Seite 617-636 volume:386 year:2021 number:3 day:04 month:10 pages:617-636
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Rat Lung development Lipopolysaccharide (LPS) CD26/DPP4 Immune cells
dewey-raw	570
isfreeaccess_bool	true
container_title	Cell & tissue research
authorswithroles_txt_mv	Schmiedl, Andreas @@aut@@ Wagener, Inga @@aut@@ Jungen, Meike @@aut@@ von Hörsten, Stephan @@aut@@ Stephan, Michael @@aut@@
publishDateDaySort_date	2021-10-04T00:00:00Z
hierarchy_top_id	253390516
dewey-sort	3570
id	SPR045587876
language_de	englisch
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author	Schmiedl, Andreas
spellingShingle	Schmiedl, Andreas ddc 570 bkl 42.15 misc Rat misc Lung development misc Lipopolysaccharide (LPS) misc CD26/DPP4 misc Immune cells Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
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topic_title	570 610 ASE 42.15 bkl Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency Rat (dpeaa)DE-He213 Lung development (dpeaa)DE-He213 Lipopolysaccharide (LPS) (dpeaa)DE-He213 CD26/DPP4 (dpeaa)DE-He213 Immune cells (dpeaa)DE-He213
topic	ddc 570 bkl 42.15 misc Rat misc Lung development misc Lipopolysaccharide (LPS) misc CD26/DPP4 misc Immune cells
topic_unstemmed	ddc 570 bkl 42.15 misc Rat misc Lung development misc Lipopolysaccharide (LPS) misc CD26/DPP4 misc Immune cells
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title	Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
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title_full	Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
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author_browse	Schmiedl, Andreas Wagener, Inga Jungen, Meike von Hörsten, Stephan Stephan, Michael
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title_sort	lung development and immune status under chronic lps exposure in rat pups with and without cd26/dpp4 deficiency
title_auth	Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
abstract	Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. © The Author(s) 2021
abstractGer	Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. © The Author(s) 2021
abstract_unstemmed	Abstract Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of $ CD4^{+} %$ CD25^{+} $ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 $ T^{+} $ cells in $ CD26^{+} $ pups, and a significantly higher percentage of monocytes in $ CD26^{−} $ pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in $ CD26^{−} $ pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition. © The Author(s) 2021
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container_issue	3
title_short	Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
url	https://dx.doi.org/10.1007/s00441-021-03522-8
remote_bool	true
author2	Wagener, Inga Jungen, Meike von Hörsten, Stephan Stephan, Michael
author2Str	Wagener, Inga Jungen, Meike von Hörsten, Stephan Stephan, Michael
ppnlink	253390516
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isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1007/s00441-021-03522-8
up_date	2024-07-03T16:59:17.723Z
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Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency

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