15-epi-Lipoxin A₄, Resolvin D2, and Resolvin D3 Induce NF-κB Regulators in Bacterial Pneumonia.

ABSTRACT: Specialized proresolving mediators (SPMs) decrease NF-κB activity to prevent excessive tissue damage and promote the resolution of acute inflammation. Mechanisms for NF-κB regulation by SPMs remain to be determined. In this study, after LPS challenge, the SPMs 15-epi-lipoxin A₄ (15-epi-LXA₄), resolvin D1, resolvin D2, resolvin D3, and 17-epi-resolvin D1 were produced in vivo in murine lungs. In LPS-activated human bronchial epithelial cells, select SPMs increased expression of the NF-κB regulators A20 and single Ig IL-1R-related molecule (SIGIRR). Of interest, 15-epi-LXA₄ induced A20 and SIGIRR in an lipoxin A₄ receptor/formyl peptide receptor 2 (ALX/FPR2) receptor-dependent manner in epithelial cells and in murine pneumonia. This S

SUBMITTER: Sham HP 

PROVIDER: S-EPMC5906795 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature