tetano
Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol. 2013 Apr 26. [Epub ahead of print]
FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.
Gally F, Kosmider B, Weaver MR, Pate KM, Hartshorn KL, Oberley-Deegan RE.
Source
1National Jewish Health.
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. As a transporter of fatty acids, we speculate that FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and WT mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils when compared to 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.
PMID:
23624787
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23624787
FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.
Gally F, Kosmider B, Weaver MR, Pate KM, Hartshorn KL, Oberley-Deegan RE.
Source
1National Jewish Health.
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. As a transporter of fatty acids, we speculate that FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and WT mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils when compared to 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.
PMID:
23624787
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23624787