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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Inflammation 2014 ; 37 (3): 809-17 Nephropedia Template TP
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Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A #MMPMID24385240
Shi X; Shi Z; Huang H; Zhu H; Zhou P; Zhu H; Ju D
Inflammation 2014[Jun]; 37 (3): 809-17 PMID24385240show ga
Influenza A virus pandemics and emerging antiviral resistance highlight the urgent need for novel generic pharmacological strategies that reduce both viral replication and inflammation of the lung. We have previously investigated the therapeutic efficacy of recombinant human catalase (rhCAT) against viral pneumonia in mice, but the protection mechanisms involved were not explored. In the present study, we have performed a more in-depth analysis covering survival, lung inflammation, immune cell responses, production of cytokines, and inflammation signaling pathways in mice. Male imprinting control region mice were infected intranasally with high pathogenicity (H1N1) influenza A virus followed by treatment with recombinant human catalase. The administration of rhCAT resulted in a significant reduction in inflammatory cell infiltration (e.g., macrophages and neutrophils), inflammatory cytokine levels (e.g., IL-2, IL-6, TNF-alpha, IFN-gamma), the level of the intercellular adhesion molecule 1 chemokine and the mRNA levels of toll-like receptors TLR-4, TLR-7, and NF-kappaB, as well as partially maintaining the activity of the antioxidant enzymes system. These findings indicated that rhCAT might play a key protective role in viral pneumonia of mice via suppression of inflammatory immune responses.
|Animals[MESH]
|Catalase/genetics/*pharmacology[MESH]
|Cytokines/biosynthesis/blood/genetics[MESH]
|Humans[MESH]
|Inflammation/drug therapy[MESH]
|Influenza A Virus, H1N1 Subtype/*pathogenicity[MESH]