Ross M Maltz1,2,3, Jeremy Keirsey4, Sandra C Kim1,5, Amy R Mackos6, Raad Z Gharaibeh7,8, Cathy C Moore7, Jinyu Xu2, Arpad Somogyi4, Michael T Bailey2,3. 1. Division of Pediatric Gastroenterology, Nationwide Children's Hospital. 2. Center for Microbial Pathogenesis, The Research Institute, Nationwide Children's Hospital. 3. Department of Pediatrics, The Ohio State University College of Medicine. 4. Campus Chemical Instrumentation Center Mass Spec and Proteomics, The Ohio State University, Columbus, OH. 5. Department of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, PA. 6. College of Nursing, The Ohio State University, Columbus, OH. 7. Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte. 8. Bioinformatics Services Division, Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Kannapolis, NC.
Abstract
OBJECTIVES: Gastrointestinal disorders, such as inflammatory bowel diseases (IBDs) and functional gastrointestinal disorders (FGIDs), involve disrupted homeostatic interactions between the microbiota and the host. Both disorders are worsened during stress, and in laboratory mice, stress exposure has been shown to change the composition of the gut microbiome. Stress-induced changes to the microbiome exacerbate intestinal inflammation and alter intestinal motility in mice. It is, however, not yet known whether microbiota-derived short-chain fatty acids (butyrate, propionate, and acetate) and their receptors contribute to this effect. METHODS: Mice were exposed to a social disruption stress, or left undisturbed as a control. After the first stress exposure, mice were orally challenged with Citrobacter rodentium or with vehicle. The levels of short-chain fatty acids (SCFAs) were measured using gas chromatography-mass spectrometry. SCFA receptors were measured via real-time polymerase chain reaction. Microbial community composition was assessed using 16S rRNA gene sequencing. RESULTS: Stress exposure reduced colonic SCFA levels. Stress exposure and C rodentium, however, significantly increased SCFA levels and changed the expression of SCFA receptors. The levels of SCFAs did not correlate with the severity of colonic inflammation, but the colonic expression of the SCFA receptor GPR41 was positively associated with inflammatory cytokines and colonic histopathology scores. The relative abundances of several taxa of colonic bacteria were significantly changed by stress exposure, including SCFA producers. CONCLUSIONS: Social stress can have a significant effect on infection-induced colonic inflammation, and stress-induced changes in microbial-produced metabolites and their receptors may be involved.
OBJECTIVES:Gastrointestinal disorders, such as inflammatory bowel diseases (IBDs) and functional gastrointestinal disorders (FGIDs), involve disrupted homeostatic interactions between the microbiota and the host. Both disorders are worsened during stress, and in laboratory mice, stress exposure has been shown to change the composition of the gut microbiome. Stress-induced changes to the microbiome exacerbate intestinal inflammation and alter intestinal motility in mice. It is, however, not yet known whether microbiota-derived short-chain fatty acids (butyrate, propionate, and acetate) and their receptors contribute to this effect. METHODS:Mice were exposed to a social disruption stress, or left undisturbed as a control. After the first stress exposure, mice were orally challenged with Citrobacter rodentium or with vehicle. The levels of short-chain fatty acids (SCFAs) were measured using gas chromatography-mass spectrometry. SCFA receptors were measured via real-time polymerase chain reaction. Microbial community composition was assessed using 16S rRNA gene sequencing. RESULTS:Stress exposure reduced colonicSCFA levels. Stress exposure and C rodentium, however, significantly increased SCFA levels and changed the expression of SCFA receptors. The levels of SCFAs did not correlate with the severity of colonic inflammation, but the colonic expression of the SCFA receptor GPR41 was positively associated with inflammatory cytokines and colonic histopathology scores. The relative abundances of several taxa of colonic bacteria were significantly changed by stress exposure, including SCFA producers. CONCLUSIONS: Social stress can have a significant effect on infection-induced colonic inflammation, and stress-induced changes in microbial-produced metabolites and their receptors may be involved.
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