Tuberculosis Research Today is a free monthly online journal that collates and summarizes the latest research about Tuberculosis, including details on symptoms, causes, treatment, pulmonary, mycobacterium.

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

Branger J, Leemans JC, Florquin S, Speelman P, Golenbock DT, van der Poll T

Department of Experimental Internal Medicine, Academic Medical Center, Room F4-222, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. J.Branger@amc.uva.nl

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.

Published 4 July 2005 in Clin Immunol, 116(2): 174-81.
Full-text of this article is available online (may require subscription).

© 2004-2008 Tuberculosis Research Today. All Rights Reserved.