Lipopolysaccharide binding protein-deficient mice have a normal defense against pulmonary mycobacterial infection |
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Authors: | Branger Judith Leemans Jaklien C Florquin Sandrine Speelman Peter Golenbock Douglas T van der Poll Tom |
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Institution: | 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 |
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Abstract: | 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. |
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Keywords: | Tuberculosis Lipopolysaccharide binding protein Inflammation Innate host defense Murine model |
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