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The investigation of the upstream events that initiate inflammatory responses has a very important role in the illumination of the mechanisms of intracerebral hemorrhage(ICH)-induced secondary inflammatory brain injury. The formation of novel TLR2/TLR4 heterodimer after ICH detected by the western blot, immunoprecipitation and immunofluorescence technologies has strongly contributed to such advance. Using the in vivo and in vitro ICH model, we revealed the assemble of TLR2/TLR4 heterodimer mediated inflammatory injury only can be triggered by the hemoglobin(Hb) via the myeloid differentiation primary response gene 88(MyD88), but not toll/IR-1(TIR)-domain-containing adaptor protein inducing interferon-beta(TRIF). And the mutation site at the MyD88 Arg196 abolished the TLR2/TLR4 heterodimerization. Together, our findings not only further explain the upstream events that initiate inflammatory responses following ICH, but also provide a novel target-interfering with the assembly of TLR2/TLR4 heterodimer-for developing an effective treatment of ICH.

A novel theraputic target for intracerebral hemorrhage: interfering with the TLR2/TLR4 heterodimerization