| First Author | Branger J | Year | 2005 |
| Journal | Clin Immunol | Volume | 116 |
| Issue | 2 | Pages | 174-81 |
| PubMed ID | 15993364 | Mgi Jnum | J:99345 |
| Mgi Id | MGI:3582010 | Doi | 10.1016/j.clim.2005.03.014 |
| Citation | Branger J, et al. (2005) Lipopolysaccharide binding protein-deficient mice have a normal defense against pulmonary mycobacterial infection. Clin Immunol 116(2):174-181 |
| abstractText | 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. |
