Abstract
Although gut microbiota and early life events are likely involved in the development of irritable bowel syndrome (IBS), it remains unclear how these factors interact in the pathophysiology of IBS. In the present study, using rats subjected to maternal separation (MS) as a model of IBS, we investigated interrelationships among gut microbiota, stress susceptibility and intestinal permeability, and examined the effect of the probiotic Bifidobacterium bifidum G9-1 (BBG9-1) on those interrelationships. When compared with the controls at postnatal day 20, MS rats showed hypercorticosteronemia, enhanced intestinal permeability and changes in gut microbiota structure. All of these changes in MS rats were prevented by treatment with BBG9-1. Although the gut microbiota profile and basal serum corticosterone level did not differ between MS and control rats at postnatal day 56, MS rats showed hypersensitivity to restraint stress in terms of serum corticosterone level and fecal frequency. However, such hypersensitivity was not observed in MS rats treated with BBG9-1. These findings suggest that MS initiates the link between gut microbiota alteration and hypersensitivity to stress and that the triggering of this process can be prevented by the treatment with the probiotic BBG9-1.
Highlights
Gut microbiota and early life events are likely involved in the development of irritable bowel syndrome (IBS), it remains unclear how these factors interact in the pathophysiology of IBS
In the present study using the maternal separation (MS) rat model of IBS, we focused on the interrelationships existing among gut microbiota, stress susceptibility and gut pathophysiology, and examined the effect of the probiotic Bifidobacterium bifidum G9-1 (BBG9-1) in this context
BBG9-1 treatment did not completely ameliorate the MS-induced inhibition of body growth, no significant difference in body weight was evident between control and MSB rats, suggesting that BBG9-1 treatment had at least a partly preventive effect on MS-induced inhibition of body growth
Summary
Gut microbiota and early life events are likely involved in the development of irritable bowel syndrome (IBS), it remains unclear how these factors interact in the pathophysiology of IBS. Much attention has recently been paid to the gut microbiota in IBS patients because its alteration importantly affects homeostasis of the mucosal barrier, gut sensorimotor function and the brain-gut axis[3,4,5] In this context, probiotics have been applied as therapeutic drugs to normalize microbiota imbalance, there is still no evidence that they have significant therapeutic effectiveness in patients with IBS6–8. Rodents subjected to neonatal maternal separation (MS) constitute a well-established model that exhibits features similar to those of IBS in humans, such as visceral hyperalgesia and enhanced colonic motility in response to acute stress[13,14,15] As seen in this animal model, it is known that childhood abuse is closely associated with the development of functional gastrointestinal diseases such as functional dyspepsia[16] and IBS17. In the present study using the MS rat model of IBS, we focused on the interrelationships existing among gut microbiota, stress susceptibility and gut pathophysiology, and examined the effect of the probiotic BBG9-1 in this context
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