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results indicate that CXCL5 and MMPs contribute to the resistance to pneumococcal infection in mice.
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Identify Cxcl5 as a novel target of AHR-mediated gene expression in primary mouse keratinocytes.
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Parenchymal polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), have a positive correlation with IL1a, IL8, CXCL5, and Mip-1a, suggesting they may attract PMN-MDSC into the tumor
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These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11beta-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.
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IL-17RA regulates CXL-1 and 5 production in the lungs during the adaptive response.
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STAT3 is required for maximal OSM-induced CXCL5 expression.
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CXCL5 has a role in neutrophil recruitment in TH17-mediated glomerulonephritis
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Since adaptive villus growth occurs despite impaired CXCL5 expression and enhanced angiogenesis, this suggests that the growth of new blood vessels is not needed for resection-induced mucosal surface area expansion following massive SBR.
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CXCL5 regulates pulmonary responses to infection and plays a central role in conferring clock control of inflammation.
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findings demonstrated that CXCL1 and CXCL5 are increased in circulation with onset of T2D, are produced by islets under stress, and synergistically affect islet function, suggesting that these chemokines participate in pathogenesis of T2D.
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TLR2-induced epithelial-derived CXCL5 is critical for polymorphonuclear leukocyte-driven destructive inflammation in pulmonary tuberculosis.
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data suggest that CXCL6 contributes to experimental pulmonary fibrosis, and CXCL6 inhibition might be used to reduce lung toxicity associated with bleomycin treatment.
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Our data suggest that the differential regulation of the chemokine CXCL5 between osteoblasts and endothelial cells upon FGF2 treatment is involved in Hematopoietic stem cell mobilization from the osteoblast niche or bone marrow to peripheral blood.
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CXCL5 modulated macrophage activation, increased expression of the cholesterol efflux regulatory protein ABCA1, and enhanced cholesterol efflux activity in macrophages.
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The omentum is the main site of early neutrophil entry into the peritoneal cavity, where the action of CXCL5 synergizes with matrix metalloproteinases MMP-2 and -9 to promote neutrophil migration during the inflammatory process.
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CXCL5-dependent signaling cascades are essential for the recruitment of macrophages to the lungs upon subacute second hand smoke exposure.
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Cxcr2, Cxcl5, and commensal bacteria have critical roles in regulation of the IL-17/G-CSF axis and neutrophil homeostasis at mucosal sites
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In a mouse model of lung ischemia-induced angiogenesis, LIX predominates in eliciting a pro-angiogenic phenotype among the three ELR+ CXC chemokines (KC, LIX, and MIP-2) studied.
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regulates chemokine scavenging and pulmonary host defense to bacterial infection
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The villus growth observed in resection-induced adaptation is associated with increased expression of the chemokine CXCL5 within the lamina propria.
