| LFA-1 and MAC-1 mediate pulmonary recruitment of neutrophils and tissue damage in abdominal sepsis. | |
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MedLine Citation:
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PMID: 18197144 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neutrophil-mediated lung damage is an insidious feature in septic patients, although the adhesive mechanisms behind pulmonary recruitment of neutrophils in polymicrobial sepsis remain elusive. The aim of the present study was to define the role of lymphocyte function antigen-1 (LFA-1) and membrane-activated complex 1 (Mac-1) in septic lung injury. Pulmonary edema, bronchoalveolar infiltration of neutrophils, levels of myeloperoxidase, and CXC chemokines were determined after cecal ligation and puncture (CLP). Mice were treated with monoclonal antibodies directed against LFA-1 and Mac-1 before CLP induction. Cecal ligation and puncture induced clear-cut pulmonary damage characterized by edema formation, neutrophil infiltration, and increased levels of CXC chemokines in the lung. Notably, immunoneutralization of LFA-1 or Mac-1 decreased CLP-induced neutrophil recruitment in the bronchoalveolar space by more than 64%. Moreover, functional inhibition of LFA-1 and Mac-1 abolished CLP-induced lung damage and edema. However, formation of CXC chemokines in the lung was intact in mice pretreated with the anti-LFA-1 and anti-Mac-1 antibodies. Our data demonstrate that both LFA-1 and Mac-1 regulate pulmonary infiltration of neutrophils and lung edema associated with abdominal sepsis. Thus, these novel findings suggest that LFA-1 or Mac-1 may serve as targets to protect against lung injury in polymicrobial sepsis. |
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Authors:
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Muhammad Asaduzzaman; Su Zhang; Shahram Lavasani; Yusheng Wang; Henrik Thorlacius |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Shock (Augusta, Ga.) Volume: 30 ISSN: 1540-0514 ISO Abbreviation: Shock Publication Date: 2008 Sep |
Date Detail:
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Created Date: 2008-09-02 Completed Date: 2008-12-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9421564 Medline TA: Shock Country: United States |
Other Details:
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Languages: eng Pagination: 254-9 Citation Subset: IM |
Affiliation:
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Department of Surgery, Malmö University Hospital, Lund University, Malmö, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Chemokines / metabolism* Edema / immunology Gene Expression Regulation* Humans Leukocytes / microbiology Lung / immunology, metabolism* Lung Injury Lymphocyte Function-Associated Antigen-1 / biosynthesis* Macrophage-1 Antigen / biosynthesis* Male Mice Mice, Inbred C57BL Models, Biological Neutrophils / immunology, metabolism* Sepsis / blood*, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Chemokines; 0/Lymphocyte Function-Associated Antigen-1; 0/Macrophage-1 Antigen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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