Lipoxin A4, a 5-lipoxygenase pathway metabolite, modulates immune response during acute respiratory tularemia.

ABSTRACT: Respiratory infection with Francisella tularensis (Ft) is characterized by a muted, acute host response, followed by sepsis-like syndrome that results in death. Infection with Ft establishes a principally anti-inflammatory environment that subverts host-cell death programs to facilitate pathogen replication. Although the role of cytokines has been explored extensively, the role of eicosanoids in tularemia pathogenesis is not fully understood. Given that lipoxin A₄ (LXA₄) has anti-inflammatory properties, we investigated whether this lipid mediator affects host responses manifested early during infection. The addition of exogenous LXA₄ inhibits PGE₂ release by Ft-infected murine monocytes in vitro and diminishes apoptotic cell death. Tularemia pat

SUBMITTER: Singh A 

PROVIDER: S-EPMC5235906 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature