B7H3 ameliorates LPS-induced acute lung injury via attenuation of neutrophil migration and infiltration
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by an excessive inflammatory response within the lungs and severely impaired gas exchange resulting from alveolar-capillary barrier disruption and pulmonary edema. The costimulatory protein B7H3 functions as bot...
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| Veröffentlicht in: | Scientific reports 2016-08, Vol.6 (1), p.31284-31284, Article 31284 |
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| description | Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by an excessive inflammatory response within the lungs and severely impaired gas exchange resulting from alveolar-capillary barrier disruption and pulmonary edema. The costimulatory protein B7H3 functions as both a costimulator and coinhibitor to regulate the adaptive and innate immune response, thus participating in the development of microbial sepsis and pneumococcal meningitis. However, it is unclear whether B7H3 exerts a beneficial or detrimental role during ALI. In the present study we examined the impact of B7H3 on pulmonary inflammatory response, polymorphonuclear neutrophil (PMN) influx and lung tissue damage in a murine model of lipopolysaccharide (LPS)-induced direct ALI. Treatment with B7H3 protected mice against LPS-induced ALI, with significantly attenuated pulmonary PMN infiltration, decreased lung myeloperoxidase (MPO) activity, reduced bronchoalveolar lavage fluid (BALF) protein content and ameliorated lung pathological changes. In addition, B7H3 significantly diminished LPS-stimulated PMN chemoattractant CXCL2 production by inhibiting NF-κB p65 phosphorylation and substantially attenuated LPS-induced PMN chemotaxis and transendothelial migration by down-regulating CXCR2 and Mac-1 expression. These results demonstrate that B7H3 substantially ameliorates LPS-induced ALI and this protection afforded by B7H3 is predominantly associated with its inhibitory effect on pulmonary PMN migration and infiltration. |
| doi_str_mv | 10.1038/srep31284 |
| format | Article |
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Paul ; Wang, Jiang Huai ; Wang, Jian</creator><creatorcontrib>Li, Yan ; Huang, Jie ; Foley, Niamh M. ; Xu, Yunyun ; Li, Yi Ping ; Pan, Jian ; Redmond, H. Paul ; Wang, Jiang Huai ; Wang, Jian</creatorcontrib><description>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by an excessive inflammatory response within the lungs and severely impaired gas exchange resulting from alveolar-capillary barrier disruption and pulmonary edema. The costimulatory protein B7H3 functions as both a costimulator and coinhibitor to regulate the adaptive and innate immune response, thus participating in the development of microbial sepsis and pneumococcal meningitis. However, it is unclear whether B7H3 exerts a beneficial or detrimental role during ALI. In the present study we examined the impact of B7H3 on pulmonary inflammatory response, polymorphonuclear neutrophil (PMN) influx and lung tissue damage in a murine model of lipopolysaccharide (LPS)-induced direct ALI. Treatment with B7H3 protected mice against LPS-induced ALI, with significantly attenuated pulmonary PMN infiltration, decreased lung myeloperoxidase (MPO) activity, reduced bronchoalveolar lavage fluid (BALF) protein content and ameliorated lung pathological changes. In addition, B7H3 significantly diminished LPS-stimulated PMN chemoattractant CXCL2 production by inhibiting NF-κB p65 phosphorylation and substantially attenuated LPS-induced PMN chemotaxis and transendothelial migration by down-regulating CXCR2 and Mac-1 expression. These results demonstrate that B7H3 substantially ameliorates LPS-induced ALI and this protection afforded by B7H3 is predominantly associated with its inhibitory effect on pulmonary PMN migration and infiltration.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep31284</identifier><identifier>PMID: 27515382</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/31 ; 13/95 ; 631/250/256/1980 ; 692/420/254 ; Acute Lung Injury - chemically induced ; Acute Lung Injury - metabolism ; Acute Lung Injury - pathology ; Acute Lung Injury - prevention & control ; Alveoli ; Animal models ; Animals ; B7 Antigens - pharmacology ; Bronchus ; Chemotaxis ; Costimulator ; CXCR2 protein ; Edema ; Gas exchange ; Humanities and Social Sciences ; Immune response ; Infiltration ; Inflammation ; Innate immunity ; Leukocyte migration ; Leukocytes (polymorphonuclear) ; Lipopolysaccharides ; Lipopolysaccharides - toxicity ; Lung - metabolism ; Lung - pathology ; Lungs ; Mac1 protein ; Male ; Meningitis ; Mice ; Mice, Inbred BALB C ; multidisciplinary ; Neutrophil Infiltration - drug effects ; Neutrophils ; Neutrophils - metabolism ; Neutrophils - pathology ; Peroxidase ; Phosphorylation ; Respiratory distress syndrome ; Respiratory therapy ; Rodents ; Science ; Sepsis</subject><ispartof>Scientific reports, 2016-08, Vol.6 (1), p.31284-31284, Article 31284</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Aug 2016</rights><rights>Copyright © 2016, The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-91d609c6ab1eedc2b99ff0be549e88ce20e45023e4d8c99c9d90fa498c1c74943</citedby><cites>FETCH-LOGICAL-c438t-91d609c6ab1eedc2b99ff0be549e88ce20e45023e4d8c99c9d90fa498c1c74943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4981866/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4981866/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27907,27908,41103,42172,51559,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27515382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Huang, Jie</creatorcontrib><creatorcontrib>Foley, Niamh M.</creatorcontrib><creatorcontrib>Xu, Yunyun</creatorcontrib><creatorcontrib>Li, Yi Ping</creatorcontrib><creatorcontrib>Pan, Jian</creatorcontrib><creatorcontrib>Redmond, H. Paul</creatorcontrib><creatorcontrib>Wang, Jiang Huai</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><title>B7H3 ameliorates LPS-induced acute lung injury via attenuation of neutrophil migration and infiltration</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by an excessive inflammatory response within the lungs and severely impaired gas exchange resulting from alveolar-capillary barrier disruption and pulmonary edema. The costimulatory protein B7H3 functions as both a costimulator and coinhibitor to regulate the adaptive and innate immune response, thus participating in the development of microbial sepsis and pneumococcal meningitis. However, it is unclear whether B7H3 exerts a beneficial or detrimental role during ALI. In the present study we examined the impact of B7H3 on pulmonary inflammatory response, polymorphonuclear neutrophil (PMN) influx and lung tissue damage in a murine model of lipopolysaccharide (LPS)-induced direct ALI. Treatment with B7H3 protected mice against LPS-induced ALI, with significantly attenuated pulmonary PMN infiltration, decreased lung myeloperoxidase (MPO) activity, reduced bronchoalveolar lavage fluid (BALF) protein content and ameliorated lung pathological changes. In addition, B7H3 significantly diminished LPS-stimulated PMN chemoattractant CXCL2 production by inhibiting NF-κB p65 phosphorylation and substantially attenuated LPS-induced PMN chemotaxis and transendothelial migration by down-regulating CXCR2 and Mac-1 expression. These results demonstrate that B7H3 substantially ameliorates LPS-induced ALI and this protection afforded by B7H3 is predominantly associated with its inhibitory effect on pulmonary PMN migration and infiltration.</description><subject>13</subject><subject>13/31</subject><subject>13/95</subject><subject>631/250/256/1980</subject><subject>692/420/254</subject><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - pathology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Alveoli</subject><subject>Animal models</subject><subject>Animals</subject><subject>B7 Antigens - pharmacology</subject><subject>Bronchus</subject><subject>Chemotaxis</subject><subject>Costimulator</subject><subject>CXCR2 protein</subject><subject>Edema</subject><subject>Gas exchange</subject><subject>Humanities and Social Sciences</subject><subject>Immune response</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Innate immunity</subject><subject>Leukocyte migration</subject><subject>Leukocytes (polymorphonuclear)</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Mac1 protein</subject><subject>Male</subject><subject>Meningitis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>multidisciplinary</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophils</subject><subject>Neutrophils - metabolism</subject><subject>Neutrophils - pathology</subject><subject>Peroxidase</subject><subject>Phosphorylation</subject><subject>Respiratory distress syndrome</subject><subject>Respiratory therapy</subject><subject>Rodents</subject><subject>Science</subject><subject>Sepsis</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkV1rFDEUhoMotrS98A9IwBsVps3XzCY3ghZtCwsW1OuQzZyZZplJ1nwU-u-NTLtsNTcJ5zx5z5u8CL2h5JwSLi9ShB2nTIoX6JgR0TaMM_by4HyEzlLakrpapgRVr9ERW7W05ZIdo_HL6ppjM8PkQjQZEl7f_mic74uFHhtbMuCp-BE7vy3xAd87g03O4IvJLngcBuyh5Bh2d27CsxvjUje-r1cGN-WlcIpeDWZKcPa4n6Bf377-vLxu1t-vbi4_rxsruMyNon1HlO3MhgL0lm2UGgaygVYokNICIyBawjiIXlqlrOoVGYxQ0lK7EkrwE_Rp0d2VzVwVwFcDk95FN5v4oINx-nnHuzs9hntdNajsuirw_lEght8FUtazSxamyXgIJWkqKa3f2HWkou_-QbehRF-fp6kinFeSq0p9WCgbQ6phDXszlOi_Cep9gpV9e-h-Tz7lVYGPC5Bqy48QD0b-p_YHlVimzA</recordid><startdate>20160812</startdate><enddate>20160812</enddate><creator>Li, Yan</creator><creator>Huang, Jie</creator><creator>Foley, Niamh M.</creator><creator>Xu, Yunyun</creator><creator>Li, Yi Ping</creator><creator>Pan, Jian</creator><creator>Redmond, H. 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Paul ; Wang, Jiang Huai ; Wang, Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-91d609c6ab1eedc2b99ff0be549e88ce20e45023e4d8c99c9d90fa498c1c74943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>13</topic><topic>13/31</topic><topic>13/95</topic><topic>631/250/256/1980</topic><topic>692/420/254</topic><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - pathology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Alveoli</topic><topic>Animal models</topic><topic>Animals</topic><topic>B7 Antigens - pharmacology</topic><topic>Bronchus</topic><topic>Chemotaxis</topic><topic>Costimulator</topic><topic>CXCR2 protein</topic><topic>Edema</topic><topic>Gas exchange</topic><topic>Humanities and Social Sciences</topic><topic>Immune response</topic><topic>Infiltration</topic><topic>Inflammation</topic><topic>Innate immunity</topic><topic>Leukocyte migration</topic><topic>Leukocytes (polymorphonuclear)</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Mac1 protein</topic><topic>Male</topic><topic>Meningitis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>multidisciplinary</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>Neutrophils</topic><topic>Neutrophils - metabolism</topic><topic>Neutrophils - pathology</topic><topic>Peroxidase</topic><topic>Phosphorylation</topic><topic>Respiratory distress syndrome</topic><topic>Respiratory therapy</topic><topic>Rodents</topic><topic>Science</topic><topic>Sepsis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Huang, Jie</creatorcontrib><creatorcontrib>Foley, Niamh M.</creatorcontrib><creatorcontrib>Xu, Yunyun</creatorcontrib><creatorcontrib>Li, Yi Ping</creatorcontrib><creatorcontrib>Pan, Jian</creatorcontrib><creatorcontrib>Redmond, H. 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Paul</au><au>Wang, Jiang Huai</au><au>Wang, Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B7H3 ameliorates LPS-induced acute lung injury via attenuation of neutrophil migration and infiltration</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-08-12</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>31284</spage><epage>31284</epage><pages>31284-31284</pages><artnum>31284</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by an excessive inflammatory response within the lungs and severely impaired gas exchange resulting from alveolar-capillary barrier disruption and pulmonary edema. The costimulatory protein B7H3 functions as both a costimulator and coinhibitor to regulate the adaptive and innate immune response, thus participating in the development of microbial sepsis and pneumococcal meningitis. However, it is unclear whether B7H3 exerts a beneficial or detrimental role during ALI. In the present study we examined the impact of B7H3 on pulmonary inflammatory response, polymorphonuclear neutrophil (PMN) influx and lung tissue damage in a murine model of lipopolysaccharide (LPS)-induced direct ALI. Treatment with B7H3 protected mice against LPS-induced ALI, with significantly attenuated pulmonary PMN infiltration, decreased lung myeloperoxidase (MPO) activity, reduced bronchoalveolar lavage fluid (BALF) protein content and ameliorated lung pathological changes. In addition, B7H3 significantly diminished LPS-stimulated PMN chemoattractant CXCL2 production by inhibiting NF-κB p65 phosphorylation and substantially attenuated LPS-induced PMN chemotaxis and transendothelial migration by down-regulating CXCR2 and Mac-1 expression. These results demonstrate that B7H3 substantially ameliorates LPS-induced ALI and this protection afforded by B7H3 is predominantly associated with its inhibitory effect on pulmonary PMN migration and infiltration.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27515382</pmid><doi>10.1038/srep31284</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/31 13/95 631/250/256/1980 692/420/254 Acute Lung Injury - chemically induced Acute Lung Injury - metabolism Acute Lung Injury - pathology Acute Lung Injury - prevention & control Alveoli Animal models Animals B7 Antigens - pharmacology Bronchus Chemotaxis Costimulator CXCR2 protein Edema Gas exchange Humanities and Social Sciences Immune response Infiltration Inflammation Innate immunity Leukocyte migration Leukocytes (polymorphonuclear) Lipopolysaccharides Lipopolysaccharides - toxicity Lung - metabolism Lung - pathology Lungs Mac1 protein Male Meningitis Mice Mice, Inbred BALB C multidisciplinary Neutrophil Infiltration - drug effects Neutrophils Neutrophils - metabolism Neutrophils - pathology Peroxidase Phosphorylation Respiratory distress syndrome Respiratory therapy Rodents Science Sepsis |
| title | B7H3 ameliorates LPS-induced acute lung injury via attenuation of neutrophil migration and infiltration |
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