Lipopolysaccharide binding protein-deficient mice have a normal defense against pulmonary mycobacterial infection.

Lipopolysaccharide (LPS) binding protein (LBP) facilitates the transfer of LPS of Gram-negative bacteria to the pattern recognition receptor CD14, resulting in activation of immunocompetent cells. LBP can also facilitate the binding of lipoarabinomannan, a major cell wall component of mycobacteria, to immune cells. To determine the role of LBP in the immune response to pulmonary Mycobacterium tuberculosis infection, LBP gene-deficient (−/−) and normal wild-type (WT) mice were intranasally infected with M. tuberculosis. LBP−/− mice displayed a similar survival and mycobacterial outgrowth in lungs and liver, although they demonstrated a reduced lymphocyte recruitment and activation during the early stages of infection. The clearance of pulmonary infection with the non-pathogenic M. smegmatis was also unaltered in LBP−/− mice. These data suggest that LBP does not contribute to an effective host response in M. tuberculosis infection.