International Immunology Advance Access originally published online on September 27, 2004
International Immunology 2004 16(11):1605-1611; doi:10.1093/intimm/dxh161
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© 2004 The Japanese Society for Immunology
LPS-binding protein-deficient mice have an impaired defense against Gram-negative but not Gram-positive pneumonia
1 Department of Experimental Internal Medicine, 2 Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS and 3 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
4 Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA
Correspondence to: J. Branger; E-mail: j.branger{at}amc.uva.nl
LPS-binding protein (LBP) can facilitate the transfer of cell wall components of both Gram-negative bacteria (LPS) and Gram-positive bacteria (lipoteichoic acid) to inflammatory cells. Although LBP is predominantly produced in the liver, recent studies have indicated that this protein is also synthesized locally in the lung by epithelial cells. To determine the role of LBP in the immune response to pneumonia, LBP gene-deficient (–/–) and normal wild-type (WT) mice were intra-nasally infected with either Streptococcus pneumoniae or Klebsiella pneumoniae, common Gram-positive and Gram-negative pathogens, respectively. Pneumococcal pneumonia was associated with a 7-fold rise in LBP concentrations in bronchoalveolar lavage fluid of WT mice; LBP–/– mice infected with S. pneumoniae showed a similar survival and a similar bacterial burden in their lungs 48 h post-infection. In Klebsiella pneumonia, however, LBP–/– mice demonstrated a diminished survival together with an enhanced bacterial outgrowth in their lungs. These data suggest that LBP is important for a protective immune response in Klebsiella pneumonia, but does not contribute to an effective host response in pneumococcal pneumonia.
Keywords: inflammation, innate immunity, LBP, mouse, pulmonary infection
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