CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions

摘要: Severe bacterial sepsis leads to a proinflammatory condition that can manifest as septic shock, multiple organ failure, and death. Neutrophils are critical for the rapid elimination of bacteria; however, role neutrophil chemoattractant CXCL1 in clearance during remains elusive. To test hypothesis is host defense sepsis, we used CXCL1-deficient mice bone marrow chimeras demonstrate importance this molecule sepsis. We plays pivotal mediating polymicrobial after cecal ligation puncture gene-deficient mice. appears be essential restricting outgrowth death derived from both hematopoietic resident cells contributed clearance. Moreover, migration, expression mediators, activation NF-κB MAPKs, upregulation adhesion ICAM-1. rIL-17 rescued impaired defenses cxcl1(-/-) important IL-17A production via Th17 differentiation. NADPH oxidase-mediated reactive oxygen species extracellular trap formation. This study reveals novel recruitment modulating T cell function neutrophil-related bactericidal functions. These studies suggest modulation levels tissues blood could reduce burden