The effects of repeated social interaction stress on behavioural and physiological parameters in a stress-sensitive mouse strain

Stress can impair the immune, endocrine and nervous systems. Such perturbations can also affect brain-gut axis communication and lead to functional gastrointestinal disorders such as irritable bowel syndrome (IBS). IBS is a common yet poorly understood disorder which is often co-morbid with anxiety and depression. As there are few mouse models of IBS, this study aimed to investigate if a short and intense social stress which involved bouts of physical interaction could induce behavioural and physiological changes similar to those observed in IBS patients in the innately anxious BALB/c mice. Male BALB/c mice were exposed for 2 h to an aggressive male intruder for acute (one-day) or chronic (six-day) stress. Behaviour was analyzed and weight monitored. Two hours post stress, trunk blood and tissues were collected. Plasma was analyzed for inflammatory cytokines and corticosterone and morphological damage to the colon was also assessed. Mice displayed either dominant or submissive status following repeated intruder exposure. Behavioural status correlated with an increase in corticosterone and pro-inflammatory cytokines in both acute and chronic submissive groups. Mice from both status groups had body weight loss coupled with mild damage to the colon. Together these data show that short-term social interaction stress exposure was able to induce behavioural and physiological impairments similar to that observed in patients with dysregulated brain-gut axis function. Moreover, these data demonstrate that social stress-based mouse models may be appropriate for interrogating the mechanisms underlying such disorders.

Research highlights▶ Mice displayed either dominant or submissive status following repeated intruder exposure. ▶ Behavioural status correlated with an increase in corticosterone and pro-inflammatory cytokines. ▶ These effects are similar to patients with a dysregulated brain-gut axis function.