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Lack of group X secreted phospholipase A₂ increases survival following pandemic H1N1 influenza infection.

Abstract
The role of Group X secreted phospholipase A2 (GX-sPLA2) during influenza infection has not been previously investigated. We examined the role of GX-sPLA2 during H1N1 pandemic influenza infection in a GX-sPLA2 gene targeted mouse (GX(-/-)) model and found that survival after infection was significantly greater in GX(-/-) mice than in GX(+/+) mice. Downstream products of GX-sPLA2 activity, PGD2, PGE2, LTB4, cysteinyl leukotrienes and Lipoxin A4 were significantly lower in GX(-/-) mice BAL fluid. Lung microarray analysis identified an earlier and more robust induction of T and B cell associated genes in GX(-/-) mice. Based on the central role of sPLA2 enzymes as key initiators of inflammatory processes, we propose that activation of GX-sPLA2 during H1N1pdm infection is an early step of pulmonary inflammation and its inhibition increases adaptive immunity and improves survival. Our findings suggest that GX-sPLA2 may be a potential therapeutic target during influenza.
AuthorsAlyson A Kelvin, Norbert Degousee, David Banner, Eva Stefanski, Alberto J Leόn, Denis Angoulvant, Stéphane G Paquette, Stephen S H Huang, Ali Danesh, Clinton S Robbins, Hossein Noyan, Mansoor Husain, Gerard Lambeau, Michael Gelb, David J Kelvin, Barry B Rubin
JournalVirology (Virology) Vol. 454-455 Pg. 78-92 (Apr 2014) ISSN: 1096-0341 [Electronic] United States
PMID24725934 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
Chemical References
  • Group X Phospholipases A2
Topics
  • Animals
  • B-Lymphocytes (immunology)
  • Disease Models, Animal
  • Gene Expression Profiling
  • Group X Phospholipases A2 (deficiency, genetics)
  • Influenza A Virus, H1N1 Subtype (immunology)
  • Lung (pathology)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microarray Analysis
  • Orthomyxoviridae Infections (pathology, virology)
  • Survival Analysis
  • T-Lymphocytes (immunology)

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