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10.1038/icb.2017.2

http://scihub22266oqcxt.onion/10.1038/icb.2017.2
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C5454315!5454315 !28074060
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suck abstract from ncbi


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pmid28074060
      Immunol+Cell+Biol 2017 ; 95 (5 ): 461-472
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  • S100A8/A9 and S100A9 reduce acute lung injury #MMPMID28074060
  • Hiroshima Y ; Hsu K ; Tedla N ; Wong SW ; Chow S ; Kawaguchi N ; Geczy CL
  • Immunol Cell Biol 2017[May]; 95 (5 ): 461-472 PMID28074060 show ga
  • S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-?, interleukin-1? (IL-1?), IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury provoked by lipopolysaccharide (LPS) challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1?, SAA3 and IL-10. Novel common pathways including increased induction of an NAD(+)-dependent protein deacetylase sirtuin-1 that may reduce NF-?B signalling, and increased STAT3 activation may reduce LPS activation. Results suggest a role for these proteins in normal homeostasis and protective mechanisms in the lung.
  • |Acute Lung Injury/genetics/*metabolism/pathology [MESH]
  • |Animals [MESH]
  • |Bronchoalveolar Lavage Fluid [MESH]
  • |Chemokine CXCL10/metabolism [MESH]
  • |Female [MESH]
  • |Gene Expression Regulation [MESH]
  • |Inflammation Mediators/metabolism [MESH]
  • |Inflammation/genetics/pathology [MESH]
  • |Lipopolysaccharides [MESH]
  • |Lung/metabolism/pathology [MESH]
  • |Lymphocytes/pathology [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |Neutrophil Infiltration [MESH]
  • |Phosphorylation [MESH]
  • |S100 Proteins/*metabolism [MESH]


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