IL18 and bacterial infectious disease: The importance of neuroimmune interactions in response to bacterial infection is further highlighted by the discovery that neurons are a key source of protective IL-18 in response to Salmonella infection.27 During such infections, enteric neurons release IL-18 to promote AMP secretion from goblet cells via a caspase 1-independent mechanism, leading to improved pathogen control (Fig. 3).27 This highlights the ENS as an important component of the host protective response and raises the question of why neurons, rather than IL-18 competent cells were key to protection.