In contrast, TLR4 knockout mice showed significantly higher bacterial burden than control animals after infection with strain 2308 [49], and the Brucella lumazine synthase [52], or the protein moiety of Omp16 [53], or both, rather than Brucella LPS, are putative ligands in TLR4-mediated protection against B. abortus. This evidence concerns the gene TLR4 and infection.