Article ; Online: FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.
American journal of physiology. Lung cellular and molecular physiology
2013 Volume 305, Issue 1, Page(s) L64–72
Abstract: ... FABP5 expression decreased following influenza A infection in WT lung tissues that corresponded ... The early inflammatory response to influenza A virus infection contributes to severe lung ... levels of H1N1-specific IgG antibodies. FABP5 deficiency greatly enhanced oxidative damage and ...
Abstract | The early inflammatory response to influenza A virus infection contributes to severe lung disease and continues to pose a serious threat to human health. The mechanisms by which inflammatory cells invade the respiratory tract remain unclear. Uncontrolled inflammation and oxidative stress cause lung damage in response to influenza A infection. We have previously shown that the fatty acid binding protein 5 (FABP5) has anti-inflammatory properties. We speculate that, as a transporter of fatty acids, FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and wild-type (WT) mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils compared with WT mice. FABP5-/- mice presented lower viral burden but lost as much weight as WT mice. The adaptive immune response was also increased in FABP5-/- mice as illustrated by the accumulation of T and B cells in the lung tissues and increased levels of H1N1-specific IgG antibodies. FABP5 deficiency greatly enhanced oxidative damage and lipid peroxidation following influenza A infection and presented with sustained tissue inflammation. Interestingly, FABP5 expression decreased following influenza A infection in WT lung tissues that corresponded to a decrease in the anti-inflammatory molecule PPAR-γ activity. In conclusion, our results demonstrate a previously unknown contribution of FABP5 to influenza A virus pathogenesis by controlling excessive oxidative damage and inflammation. This property could be exploited for therapeutic purposes. |
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MeSH term(s) | Adaptive Immunity ; Animals ; Blotting, Western ; Cells, Cultured ; Disease Susceptibility ; Enzyme-Linked Immunosorbent Assay ; Fatty Acid-Binding Proteins/physiology ; Fluorescent Antibody Technique ; Humans ; Immunoenzyme Techniques ; Immunoprecipitation ; Influenza A Virus, H1N1 Subtype/pathogenicity ; Influenza, Human/complications ; Influenza, Human/immunology ; Influenza, Human/virology ; Lipid Peroxidation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neoplasm Proteins/physiology ; Oxidative Stress ; PPAR gamma/metabolism ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction | ||||||||||
Chemical Substances | Fabp5 protein, mouse ; Fatty Acid-Binding Proteins ; Neoplasm Proteins ; PPAR gamma ; RNA, Messenger | ||||||||||
Language | English | ||||||||||
Publishing date | 2013-04-26 | ||||||||||
Publishing country | United States | ||||||||||
Document type | Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't | ||||||||||
ZDB-ID | 1013184-x | ||||||||||
ISSN | 1522-1504 ; 1040-0605 | ||||||||||
ISSN (online) | 1522-1504 | ||||||||||
ISSN | 1040-0605 | ||||||||||
DOI | 10.1152/ajplung.00276.2012 | ||||||||||
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Database | MEDical Literature Analysis and Retrieval System OnLINE |
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