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10.1165/rcmb.2015-0120OC http://scihub22266oqcxt.onion/10.1165/rcmb.2015-0120OC C4821033!4821033 !26273949     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26273949 &cmd=llinks): Failed to open stream: HTTP request failed! 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Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard-Induced Lung Injury and Fibrosis |pdf=|usr=}}{{26273949 }} gab.com Text Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard-Induced Lung Injury and Fibrosis JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=26273949 #FOAvip Nitrogen mustard (NM) is an alkylating agent known to cause extensive pulmonary injury progressing to fibrosis. This is accompanied by a persistent macrophage inflammatory response. In these studies, we characterized the phenotype of macrophages accumulating in the lung over time following NM exposure. Treatment of rats with NM (0.125 mg/kg, intratracheally) resulted in an increase in CD11b(+) macrophages in histologic sections. These cells consisted of inducible nitric oxide synthase(+) (iNOS) proinflammatory M1 macrophages, and CD68(+), CD163(+), CD206(+), YM-1(+), and arginase-II(+)antiinflammatory M2 macrophages. Although M1 macrophages were prominent 1-3 days after NM, M2 macrophages were most notable at 28 days. At this time, they were enlarged and vacuolated, consistent with a profibrotic phenotype. Flow cytometric analysis of isolated lung macrophages identified three phenotypically distinct subpopulations: mature CD11b(-), CD43(-), and CD68(+) resident macrophages, which decreased in numbers after NM; and two infiltrating (CD11b(+)) macrophage subsets: immature CD43(+) M1 macrophages and mature CD43(-) M2 macrophages, which increased sequentially. Time-related increases in M1 (iNOS, IL-12?, COX-2, TNF-?, matrix metalloproteinase-9, matrix metalloproteinase-10) and M2 (IL-10, pentraxin-2, connective tissue growth factor, ApoE) genes, as well as chemokines/chemokine receptors associated with trafficking of M1 (CCR2, CCR5, CCL2, CCL5) and M2 (CX3CR1, fractalkine) macrophages to sites of injury, were also noted in macrophages isolated from the lung after NM. The appearance of M1 and M2 macrophages in the lung correlated with NM-induced acute injury and the development of fibrosis, suggesting a potential role of these macrophage subpopulations in the pathogenic response to NM. Twit Text FOAVip Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard-Induced Lung Injury and Fibrosis ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=26273949 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26273949 #FOAvip English Wikipedia <ref>{{Cite pmid|26273949 }}</ref> Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard-Induced Lung Injury and Fibrosis #MMPMID26273949 Venosa A ; Malaviya R ; Choi H ; Gow AJ ; Laskin JD ; Laskin DL Am J Respir Cell Mol Biol 2016[Mar]; 54 (3 ): 436-46 PMID26273949 show ga Nitrogen mustard (NM) is an alkylating agent known to cause extensive pulmonary injury progressing to fibrosis. This is accompanied by a persistent macrophage inflammatory response. In these studies, we characterized the phenotype of macrophages accumulating in the lung over time following NM exposure. Treatment of rats with NM (0.125 mg/kg, intratracheally) resulted in an increase in CD11b(+) macrophages in histologic sections. These cells consisted of inducible nitric oxide synthase(+) (iNOS) proinflammatory M1 macrophages, and CD68(+), CD163(+), CD206(+), YM-1(+), and arginase-II(+)antiinflammatory M2 macrophages. Although M1 macrophages were prominent 1-3 days after NM, M2 macrophages were most notable at 28 days. At this time, they were enlarged and vacuolated, consistent with a profibrotic phenotype. Flow cytometric analysis of isolated lung macrophages identified three phenotypically distinct subpopulations: mature CD11b(-), CD43(-), and CD68(+) resident macrophages, which decreased in numbers after NM; and two infiltrating (CD11b(+)) macrophage subsets: immature CD43(+) M1 macrophages and mature CD43(-) M2 macrophages, which increased sequentially. Time-related increases in M1 (iNOS, IL-12?, COX-2, TNF-?, matrix metalloproteinase-9, matrix metalloproteinase-10) and M2 (IL-10, pentraxin-2, connective tissue growth factor, ApoE) genes, as well as chemokines/chemokine receptors associated with trafficking of M1 (CCR2, CCR5, CCL2, CCL5) and M2 (CX3CR1, fractalkine) macrophages to sites of injury, were also noted in macrophages isolated from the lung after NM. The appearance of M1 and M2 macrophages in the lung correlated with NM-induced acute injury and the development of fibrosis, suggesting a potential role of these macrophage subpopulations in the pathogenic response to NM. |*Mechlorethamine [MESH] |Animals [MESH] |Biomarkers/metabolism [MESH] |Cytokines/genetics/immunology/metabolism [MESH] |Disease Models, Animal [MESH] |Gene Expression Regulation [MESH] |Inflammation Mediators/immunology/metabolism [MESH] |Lung Injury/chemically induced/genetics/*immunology/metabolism/pathology [MESH] |Lung/*immunology/metabolism/pathology [MESH] |Macrophages/*immunology/metabolism [MESH] |Male [MESH] |Phenotype [MESH] |Pneumonia/chemically induced/genetics/*immunology/metabolism/pathology [MESH] |Pulmonary Fibrosis/chemically induced/genetics/*immunology/metabolism/pathology [MESH] |Rats, Wistar [MESH]Characterization of Distinct Macrophage Subpopulations during Nitrogen(epmc).pdf DeepDyve Pubget Overpricing