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Sökning: WFRF:(Wang Yusheng) > LFA-1 AND MAC-1 MED...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003447naa a2200337 4500
001oai:lup.lub.lu.se:e7aa3837-e525-40ef-b5a8-8e3fbfb9ddac
003SwePub
008160404s2008 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/10213612 URI
024a https://doi.org/10.1097/shk.0b013e318162c5672 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Asaduzzaman, Muhammad4 aut
2451 0a LFA-1 AND MAC-1 MEDIATE PULMONARY RECRUITMENT OF NEUTROPHILS AND TISSUE DAMAGE IN ABDOMINAL SEPSIS.
264 1b Ovid Technologies (Wolters Kluwer Health),c 2008
520 a 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.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
700a Zhang, Suu Lund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups4 aut0 (Swepub:lu)med-sza
700a Lavasani, Shahramu Lund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups4 aut0 (Swepub:lu)infl-sl8
700a Wang, Yushengu Lund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups4 aut0 (Swepub:lu)yu4833wa
700a Thorlacius, Henriku Lund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups4 aut0 (Swepub:lu)kir-hth
710a Kirurgib Forskargrupper vid Lunds universitet4 org
773t Shockd : Ovid Technologies (Wolters Kluwer Health)g 30, s. 254-259q 30<254-259x 1540-0514x 1073-2322
856u http://www.ncbi.nlm.nih.gov/pubmed/18197144?dopt=Abstracty FULLTEXT
856u http://dx.doi.org/10.1097/shk.0b013e318162c567y FULLTEXT
8564 8u https://lup.lub.lu.se/record/1021361
8564 8u https://doi.org/10.1097/shk.0b013e318162c567

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Av författaren/redakt...
Asaduzzaman, Muh ...
Zhang, Su
Lavasani, Shahra ...
Wang, Yusheng
Thorlacius, Henr ...
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MEDICIN OCH HÄLSOVETENSKAP
MEDICIN OCH HÄLS ...
och Klinisk medicin
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Shock
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Lunds universitet

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