In order to generate murine infection models mirroring clinical features of severe campylobacteriosis, researchers including our group—independently from each other—modified the microbiota in order to overcome CR, as well as LOS sensitivity via different genetic manipulations or by zinc depletion, which all in turn affect LOS/TLR-4 dependent signaling pathways [50,51,52,53,54] (Figure 4). This evidence concerns the gene TLR4 and campylobacteriosis.