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Cutting Edge |
* Department of Surgery, Klinikum rechts der Isar, and
Institute of Medical Microbiology, Immunology, and Hygiene, Technische Universität München, Munich, Germany
Toll-like receptors (TLRs) are important for the activation of
innate immune cells upon encounter of microbial pathogens. The present
study investigated the potential roles of TLR2, TLR4, and the signaling
protein myeloid differentiation factor 88 (MyD88) in polymicrobial
septic peritonitis. Whereas both TLR2 and TLR4 were dispensable for
host defense against septic peritonitis, MyD88-deficient mice were
protected in this infection model. Recruitment of neutrophils to the
septic focus and bacterial clearance were normal in MyD88-deficient
mice. In contrast, the systemic inflammatory response was strongly
attenuated in the absence of MyD88. Surprisingly, MyD88 deficiency did
not alter cytokine and chemokine production in spleen, but markedly
reduced the inflammatory response in liver and lung. Production of
monocyte chemoattractant protein-1 and macrophage-inflammatory
protein-1
was entirely independent of MyD88. These results imply a
central role of MyD88 for the systemic immune pathology of
polymicrobial sepsis and show that cytokine production in spleen and
induction of certain chemokines are MyD88
independent.
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