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10.1016/j.imlet.2011.10.009 http://scihub22266oqcxt.onion/10.1016/j.imlet.2011.10.009 C3243824!3243824 !22037624     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22037624 &cmd=llinks): Failed to open stream: HTTP request failed! 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Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza |pdf=|usr=}}{{22037624 }} gab.com Text Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza JO: Immunol Lett http://www.kidney.de/pget.php?&tw=1&pmid=22037624 #FOAvip PURPOSE: Secondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia. METHODS: C57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of Streptococcus pneumoniae serotype 3 (Sp3). RESULTS: PR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands. CONCLUSIONS: The mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection. Twit Text FOAVip Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza ????Immunol Lett http://www.kidney.de/pget.php?&tw=1&pmid=22037624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22037624 #FOAvip English Wikipedia <ref>{{Cite pmid|22037624 }}</ref> Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza #MMPMID22037624 Chen WH ; Toapanta FR ; Shirey KA ; Zhang L ; Giannelou A ; Page C ; Frieman MB ; Vogel SN ; Cross AS Immunol Lett 2012[Jan]; 141 (2 ): 227-34 PMID22037624 show ga PURPOSE: Secondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia. METHODS: C57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of Streptococcus pneumoniae serotype 3 (Sp3). RESULTS: PR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands. CONCLUSIONS: The mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection. |Animals [MESH] |Arginase/genetics/metabolism [MESH] |Cells, Cultured [MESH] |Complement Pathway, Alternative [MESH] |Disease Susceptibility [MESH] |Gene Expression Regulation [MESH] |Influenza A virus/*immunology/pathogenicity [MESH] |Intercellular Signaling Peptides and Proteins/genetics [MESH] |Interleukin-13/immunology/metabolism [MESH] |Interleukin-4/immunology/metabolism [MESH] |Lectins/genetics [MESH] |Macrophage Activation/immunology [MESH] |Macrophages, Alveolar/immunology/*metabolism/pathology/virology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Orthomyxoviridae Infections/*complications/*immunology [MESH] |Pneumococcal Infections/etiology/*immunology [MESH] |Streptococcus pneumoniae/*immunology/pathogenicity [MESH]Potential role for alternatively activated macrophages in the secondar(epmc).pdf DeepDyve Pubget Overpricing