Journal
CELL REPORTS MEDICINE
Volume 1, Issue 7, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.xcrm.2020.100124
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Categories
Funding
- NIH [P30DK052574, 1R01AI140755, 1R01AI136515, DK114007, T32 GM007200-42]
- BWF
- ICTS (Washington University)
- Wolff Professorship
- Crohn's and Colitis Foundation
- NIAID [K08 AI113184]
- AAAAI Foundation
- NIDDK [R01DK116178]
- Urology Care Foundation Research Scholars Program
- Kailash Kedia Research Scholar Award
- NIDDK Career Development Award [K01 DK115634]
- Minnesota Partnership for Biotechnology and Medical Genomics
- NCI Cancer Center Support Grant [P30 CA91842]
- ICTS/CTSA grant from the National Center for Research Resources (NCRR), NIH [UL1TR002345]
- NIH Roadmap for Medical Research
- [DK109384]
- [CA206039]
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Stress is a known trigger for flares of inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS); however, this process is not well understood. Here, we find that restraint stress in mice leads to signs of diarrhea, fecal dysbiosis, and a barrier defect via the opening of goblet-cell associated passages. Notably, stress increases host immunity to gut bacteria as assessed by immunoglobulin A (IgA)-bound gut bacteria. Stress-induced microbial changes are necessary and sufficient to elicit these effects. Moreover, similar to mice, many diarrhea-predominant IBS (IBS-D) patients from two cohorts display increased antibacterial immunity as assessed by IgA-bound fecal bacteria. This antibacterial IgA response in IBS-D correlates with somatic symptom severity and was distinct from healthy controls or IBD patients. These findings suggest that stress may play an important role in patients with IgA-associated IBS-D by disrupting the intestinal microbial community that alters gastrointestinal function and host immunity to commensal bacteria.
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