The complex interplay between stress and bacterial infections in animals

Over the past decade, an increasing awareness has arisen of the role of neuroendocrine hormones in the susceptibility of mammalian hosts to a bacterial infection. During a stress response, glucocorticoids, catecholamines and neuroendocrine factors are released into the circulation of the host. For a long time the effects of stress on the course of an infection have been exclusively ascribed to the direct effect of stress-related hormones on the immune system and the intestinal barrier function. Chronic stress is known to cause a shift from T helper 1-mediated cellular immunity toward T helper 2-mediated humoral immunity, which can influence the course of an infection and/or the susceptibility to a microorganism. Bacteria can however also respond directly to stress-related host signals. Catecholamines can alter growth, motility, biofilm formation and/or virulence of pathogens and commensal bacteria, and as a consequence influence the outcome of infections by these bacteria in many hosts. For some bacteria, such as Salmonella, Escherichia coli and Pseudomonas aeruginosa it was shown that this influence is regulated by quorum sensing mechanisms. In this manuscript an overview of how and when stress influences the outcome of bacterial infections in animals is provided