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* Infectious Diseases Section, Veterans Affairs Healthcare System, San Diego, CA 92161; and University of California School of Medicine, San Diego, CA 92093;
Division of Infectious Diseases, Center Hospitalier Universitaire Vaudois, Lausanne, Switzerland; and
Section of Infectious Diseases, Boston Medical Center, and Boston University School of Medicine, Boston, MA 01605
Polymorphonuclear leukocytes (PMN) and LPS-binding protein (LBP)
are both components of the innate immune system. LBP is a plasma
protein that binds to lipid A and enhances the biological activity of
LPS 100- to 1000-fold. Recently it was reported that LBP-deficient mice
are more susceptible to Salmonella typhimurium
infection. Here we report that LBP KO mice are more susceptible to
Salmonella peritonitis, but not to oral or i.v.
infection. LBP knockout (KO) mice responded normally to i.p. injections
of Staphylococcus aureus and casein, but not to i.p.
injection of S. typhimurium or Salmonella
LPS. Mice with a mutation in Toll-like receptor 4 (C3H/HeJ) have a
similar defect in PMN chemotaxis. In normal mice S.
typhimurium stimulated production of the CXC chemokines
macrophage inflammatory protein-2 and cytokine-induced neutrophil
chemoattractant, but levels of cytokine-induced neutrophil
chemoattractant and macrophage inflammatory protein-2 were greatly
reduced in the LBP KO mice. LBP KO mice pretreated with casein to
attract PMN in an LBP-independent manner were more resistant to
Salmonella infection, but neutropenic mice were not
protected by casein. Splenic TNF-
mRNA levels were also lower in LBP
KO than in control mice infected with Salmonella. Since
TNF- can activate PMN, LBP KO mice may have both fewer and less
active PMN in the first few hours after Salmonella are
injected, making LBP KO mice more susceptible. This work confirms the
importance of PMN in resistance to Salmonella infections
and shows that this is facilitated by LBP.
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