Bacteria living within the environs of a host (whether human or animal) are subject to stressful conditions and have to overcome them to survive.^1,2 In particular, enteric bacterial pathogens have to tolerate exposure to the acid environment of the stomach, resist the detergent-like activity of bile salts and ever decreasing oxygen concentrations as they descend the gastrointestinal tract, the presence of a competing microbial flora and the antimicrobial peptides of the epithelial surfaces they encounter. Bacteria—whether commensal, obligate or opportunist pathogens—live in a permanent state of stress and regulate their gene expression and, in the case of potential pathogens, virulence gene expression^1,2 in response to these environmental stresses.

The mammalian or avian hosts harbouring these organisms may themselves be subject to conditions that induce stress and the physiological responses that characterise that rather imprecise term. Thus, ill human patients in hospital—whether due to acute illness, infection, any form of accidental/induced trauma or animals reared and transported under some food production conditions—have a neurophysiological response to stress by the local (enteric) and systemic release of catecholamine hormones and, in particular, norepinephrine (noradrenaline) by the enteric nervous system.^3,4

It has been recognised for some time that norepinephrine potentiates bacterial growth both in vivo and in vitro and induces expression of virulence determinants in enteric pathogens, particularly Escherichia coli.^5,6 In this issue of Gut, Cogan et al⁷ (see page 1060) provide evidence that norepinephrine also regulates virulence in the important intestinal food-borne pathogen …