Human Toll-like receptor activation by pathogenic Arcobacter species.

The increase of Arcobacter spp. infection cases in humans, coupled with varying symptomatology, highlights the need to study the virulence mechanisms of these bacteria. Arcobacter butzleri can induce the release of several proinflammatory cytokines in human monocytic-derived macrophages, but the mechanism used to achieve this is still unclear. Therefore, we aimed to investigate the human innate immune response triggered by pathogenic Arcobacter spp., by studying the activation of the human Toll-like receptors (TLRs). Arcobacter skirrowii was the only species that showed the ability to activate all tested TLRs. Arcobacter cryaerophilus demonstrated to be able to activate TLR1/2, TLR4, and TLR2/6. A. butzleri hardly activated the TLRs, only TLR2/6 and TLR1/2 to a small extent. While all the Arcobacter species tested possess flagellum, as shown by motility assays and electron microscopy, only the flagellum of A. skirrowii was able to activate TLR5. The alignment of the flagellin amino acid data revealed that A. skirrowii shares a greater number of crucial amino acids for TLR5 recognition with the FliC of Salmonella than the other Arcobacter species, which might explain why A. skirrowii activates TLR5. Our results demonstrated that the activation of the different TLRs is Arcobacter species dependent, and there might be a correlation between the activation of the TLRs and the pathogenicity of the Arcobacter species.