Lowering the threshold of lung innate immune cell activation alters susceptibility to secondary bacterial superinfection.

ABSTRACT:

Background

Previous studies have shown that the interaction of CD200R, a myeloid inhibitory receptor, with its ligand, CD200, is critical in the control of innate immune activation in the lung.

Methods and results

Using a mouse model of bacterial superinfection following influenza, we show that an absence of CD200R (a negative regulator highly expressed by macrophages and dendritic cells), restricts commensal and exogenous bacterial invasiveness and completely prevents the mortality observed in wild-type mice. This benefit is due to a heightened innate immune response to influenza virus in cd200r knockout mice that limits immune pathogenesis and viral load. In wild-type mice, apoptotic cells expressing CD200 that we believe contribute to the suppressed innate immune response

SUBMITTER: Goulding J 

PROVIDER: S-EPMC3164429 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature