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Invasive Group B Streptococcal Disease of Differentiation Factor 88 in a Mouse Model Dual Role of TLR2 and Myeloid

Toll-like receptors (TLRs) are involved in pathogen recognition by the innate immune system. Different TLRs and the adaptor molecule myeloid differentiation factor 88 (MyD88) were previously shown to mediate in vitro cell activation induced by group B streptococcus (GBS). The present study examined the potential in vivo roles of TLR2 and MyD88 during infection with GBS. When pups were infected locally with a low bacterial dose, none of the TLR2- or MyD88-deﬁcient mice, but all of the wild-type ones, were able to prevent systemic spread of GBS from the initial focus. Bacterial burden was higher in MyD88- than in TLR2-deﬁcient mice, indicating a more profound defect of host defense in the former animals. In contrast, a high bacterial dose induced high level bacteremia in both mutant and wild-type mice. Under these conditions, however, TLR2 or MyD88 deﬁciency signiﬁcantly protected mice from lethality, concomitantly with decreased circulating levels of TNF- (cid:1) and IL-6. Administration of anti-TNF- (cid:1) Abs to wild-type mice could mimic the effects of TLR2 or MyD88 deﬁciency and was detrimental in the low dose model, but protective in the high dose model. In conclusion, these data highlight a dual role of TLR2 and MyD88 in the host defense against GBS sepsis and strongly suggest TNF- (cid:1) as the molecular mediator of bacterial clearance and septic shock. The Journal of Immunology, 2004, 172: 6324–6329. that MyD88 or TLR2 deﬁciency had similar effects in neonatal and adult mice in terms of their susceptibility to GBS infection.