SPLUNC1 regulation in airway epithelial cells: role of Toll-like receptor 2 signaling.

ABSTRACT:

Background

Respiratory infections including Mycoplasma pneumoniae (Mp) contribute to various chronic lung diseases. We have shown that mouse short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein was able to inhibit Mp growth. Further, airway epithelial cells increased SPLUNC1 expression upon Mp infection. However, the mechanisms underlying SPLUNC1 regulation remain unknown. In the current study, we investigated if SPLUNC1 production following Mp infection is regulated through Toll-like receptor 2 (TLR2) signaling.

Methods

Airway epithelial cell cultures were utilized to reveal the contribution of TLR2 signaling including NF-κB to SPLUNC1 production upon bacterial infection and TLR2 agonist stimulation.

Results

Mp and TLR2 agonist Pam3CSK4 increased SPLUNC

SUBMITTER: Chu HW 

PROVIDER: S-EPMC2992501 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature