Lack of the Pattern Recognition Molecule Mannose-Binding Lectin Increases Susceptibility to Influenza A Virus Infection

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Lack of the Pattern Recognition Molecule Mannose-Binding Lectin Increases Susceptibility to Influenza A Virus Infection

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dc.contributor.author White, Mitchell R
dc.contributor.author Moyo, Patience
dc.contributor.author McClear, Sheree
dc.contributor.author Thiel, Steffen
dc.contributor.author Hartshorn, Kevan L
dc.contributor.author Chang, Wei-Chuan
dc.contributor.author Takahashi, Kazue
dc.date.accessioned 2011-04-26T03:10:23Z
dc.date.issued 2010
dc.identifier.citation Chang, Wei-Chuan, Mitchell R. White, Patience Moyo, Sheree McClear, Steffen Thiel, Kevan L. Hartshorn, and Kazue Takahashi. 2010. Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection. BMC Immunology 11: 64. en_US
dc.identifier.issn 1471-2172 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4875898
dc.description.abstract Background: Mannose-binding lectin (MBL), a pattern recognition innate immune molecule, inhibits influenza A virus infection in vitro. MBL deficiency due to gene polymorphism in humans has been associated with infection susceptibility. These clinical observations were confirmed by animal model studies, in which mice genetically lacking MBL were susceptible to certain pathogens, including herpes simplex virus 2. Results: We demonstrate that MBL is present in the lung of naïve healthy wild type (WT) mice and that MBL null mice are more susceptible to IAV infection. Administration of recombinant human MBL (rhMBL) reverses the infection phenotype, confirming that the infection susceptibility is MBL-mediated. The anti-viral mechanisms of MBL include activation of the lectin complement pathway and coagulation, requiring serum factors. White blood cells (WBCs) in the lung increase in WT mice compared with MBL null mice on day 1 post-infection. In contrast, apoptotic macrophages (MΦs) are two-fold higher in the lung of MBL null mice compared with WT mice. Furthermore, MBL deficient macrophages appear to be susceptible to apoptosis in vitro. Lastly, soluble factors, which are associated with lung injury, are increased in the lungs of MBL null mice during IAV infection. These results suggest that MBL plays a key role against IAV infection. Conclusion: MBL plays a key role in clearing IAV and maintaining lung homeostasis. In addition, our findings also suggest that MBL deficiency maybe a risk factor in IAV infection and MBL may be a useful adjunctive therapy for IAV infection. en_US
dc.language.iso en_US en_US
dc.publisher BioMed Central en_US
dc.relation.isversionof doi:10.1186/1471-2172-11-64 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022599/pdf/ en_US
dash.license LAA
dc.title Lack of the Pattern Recognition Molecule Mannose-Binding Lectin Increases Susceptibility to Influenza A Virus Infection en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal BMC Immunology en_US
dash.depositing.author Takahashi, Kazue
dc.date.available 2011-04-26T03:10:23Z
dash.affiliation.other HMS^Pediatrics-Massachusetts General Hospital en_US

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