Since the C. jejuni-derived endotoxin LOS is a key player in mediating the TLR-4-driven hyperactivation of the immune cascade mounting in acute campylobacteriosis [44], it is tempting to speculate that the disease-mitigating effects of exogenous AC might have been due to the direct binding of the enteropathogenic endotoxin as also shown for LPS before as well as of binding and inactivation of the secreted pro-inflammatory mediators in vitro [31,45,46]. Here, TLR4 is linked to campylobacteriosis.