Given that the TLR-4 dependent signaling cascade induced by bacterial cell wall derived LOS is essential for C. jejuni-induced inflammation, a direct immuno-modulatory activity of AC in the amelioration of campylobacteriosis is further supported by its ability to directly inactivate bacterial LPS/LOS, and reactive oxygen radicals produced during inflammation as well as pro-inflammatory cytokines [40,53,56,57]. This evidence concerns the gene TLR4 and campylobacteriosis.