Toll-Like Receptors 2 and 4 Modulate Pulmonary Inflammation and Host Factors Mediated by Outer Membrane Vesicles Derived from Acinetobacter baumannii.

Abstract

Pneumonia due to Gram-negative bacteria is associated with high mortality.is a Gram-negative bacterium that is associated with hospital-acquired and ventilator-associated pneumonia. Bacteria have been described to release outer membrane vesicles (OMVs) that are capable of mediating systemic inflammation. The mechanism by whichOMVs mediate inflammation is not fully defined. We sought to investigate the roles that Toll-like receptors (TLRs) play inOMV-mediated pulmonary inflammation. We isolated OMVs fromcultures and intranasally introduced the OMVs into mice. Intranasal introduction ofOMVs mediated pulmonary inflammation, which is associated with neutrophil recruitment and weight loss. In addition,OMVs increased the release of several chemokines and cytokines in the mouse lungs. The proinflammatory responses were partially inhibited in TLR2- and TLR4-deficient mice compared to those of wild-type mice. This study highlights the important roles of TLRs inOMV-induced pulmonary inflammation.