Rapamycin attenuates acute lung injury induced by LPS through inhibition of Th17 cell proliferation in mice.
Ontology highlight
ABSTRACT: Th17 cells have been confirmed to increase neutrophils through cytokine secretions. ALI/ARDS are characterized as neutrophil infiltration in inflammation cases; however, there is conflicting information concerning the role of Th17 cells in ALI/ARDS, as well as their potential treatment value. We measured Th17-linear cytokines in the plasma of patients with sepsis-related ARDS. The consistently high levels of IL-17 and IL-22 in the nonsurvivors suggested that overreaction of the Th17-mediated immune response may be a risk factor for poor outcomes. Th17 linear cytokines were also increased in an LPS-induced murine model of acute lung injury, along with neutrophil accumulation. The mice that completely lacked IL-17 failed to accumulate and activate neutrophils. Lung inflammation was obviously
SUBMITTER: Yan Z
PROVIDER: S-EPMC4757870 | biostudies-literature | 2016 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA