Environmental-mediated intestinal homeostasis in neonatal mice

Culbreath, Courtney; Tanner, Scott M.; Yeramilli, Venkata A.; Berryhill, Taylor F.; Lorenz, Robin G.; Martin, Colin

doi:10.1016/j.jss.2015.04.002

Cited by 14 publications

(15 citation statements)

References 30 publications

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“…C57BL/6 mice were purchased from Jackson Laboratories (Bar Harbor, ME) and bred in our animal facility to obtain the mice used in this study. Special diets were created and administered as previously described 14 . In brief, the AhR ligand-free diet AIN-76A and AIN-76A supplemented with indole-3-carbinol (1000 parts per million) 31 were purchased from Envigo.…”

Section: Methodsmentioning

confidence: 99%

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Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function

Brawner

Yeramilli

Duck

et al. 2019

Sci Rep

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The intestinal microbiota is critical for maintaining homeostasis. Dysbiosis, an imbalance in the microbial community, contributes to the susceptibility of several diseases. Many factors are known to influence gut microbial composition, including diet. We have previously shown that fecal immunoglobulin (Ig) A levels are decreased in mice fed a diet free of aryl hydrocarbon receptor (AhR) ligands. Here, we hypothesize this IgA decrease is secondary to diet-induced dysbiosis. We assigned mice to a conventional diet, an AhR ligand-free diet, or an AhR ligand-free diet supplemented with the dietary AhR ligand indole-3-carbinol (I3C). We observed a global alteration of fecal microbiota upon dietary AhR ligand deprivation. Compared to mice on the conventional diet, family Erysipelotrichaceae was enriched in the feces of mice on the AhR ligand-free diet but returned to normal levels upon dietary supplementation with I3C. Faecalibaculum rodentium, an Erysipelotrichaceae species, depleted its growth media of AhR ligands. Cultured fecal bacteria from mice on the AhR ligand-free diet, but not the other two diets, were able to alter IgA levels in vitro, as was F. rodentium alone. Our data point to the critical role of AhR dietary ligands in shaping the composition and proper functioning of gut microbiota.

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Section: Methodsmentioning

confidence: 99%

“…We have shown previously that mice fed a diet deficient in AhR ligands have lower levels of fecal immunoglobulin (Ig) A compared with mice on a conventional chow diet 14 . IgA is the predominant antibody isotype at mucosal sites, and throughout the body, more IgA is produced than every other antibody isotype combined 15 .…”

Section: Introductionmentioning

confidence: 99%

Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function

Brawner

Yeramilli

Duck

et al. 2019

Sci Rep

Self Cite

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“…Additionally, exogenous AHR ligands activate intestinal intraepithelial lymphocytes and affect epithelial barrier function [76]. Furthermore, in animal studies, mice fed a diet deficient in AHR ligands had lower fecal IgA compared to mice consuming a regular chow diet [77]. In murine studies on peanut allergy, activating AHR pathways decreases peanut sensitization by shifting the naïve T cell population to a Treg phenotype [78,79].…”

Section: Polyamines Ahr Ligands and Gut Homeostasismentioning

confidence: 99%

The Role of the Microbiome in Food Allergy: A Review

et al. 2020

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Food allergies are common and estimated to affect 8% of children and 11% of adults in the United States. They pose a significant burden—physical, economic and social—to those affected. There is currently no available cure for food allergies. Emerging evidence suggests that the microbiome contributes to the development and manifestations of atopic disease. According to the hygiene hypothesis, children growing up with older siblings have a lower incidence of allergic disease compared with children from smaller families, due to their early exposure to microbes in the home. Research has also demonstrated that certain environmental exposures, such as a farming environment, during early life are associated with a diverse bacterial experience and reduced risk of allergic sensitization. Dysregulation in the homeostatic interaction between the host and the microbiome or gut dysbiosis appears to precede the development of food allergy, and the timing of such dysbiosis is critical. The microbiome affects food tolerance via the secretion of microbial metabolites (e.g., short chain fatty acids) and the expression of microbial cellular components. Understanding the biology of the microbiome and how it interacts with the host to maintain gut homeostasis is helpful in developing smarter therapeutic approaches. There are ongoing trials evaluating the benefits of probiotics and prebiotics, for the prevention and treatment of atopic diseases to correct the dysbiosis. However, the routine use of probiotics as an intervention for preventing allergic disease is not currently recommended. A new approach in microbial intervention is to attempt a more general modification of the gut microbiome, such as with fecal microbiota transplantation. Developing targeted bacterial therapies for food allergy may be promising for both the treatment and prevention of food allergy. Similarly, fecal microbiota transplantation is being explored as a potentially beneficial interventional approach. Overall, targeted bacterial therapies for food allergy may be promising for both the treatment and prevention of food allergy.

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“…At birth, IgAs is produced by the induction of intestinal microbial factors by AHR ligands, such as indoles (Culbreath et al . 2015). The less the immunoglobulin secreted, the lesser the intestinal barrier integrity preserves.…”

Section: The Mechanism Of Action Of Gut Bacteria In Intestinal Diseasmentioning

confidence: 99%

Gut dysbacteriosis and intestinal disease: mechanism and treatment

Meng

Zhang

Cao³

et al. 2020

J. Appl. Microbiol.

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Summary The gut microbiome functions like an endocrine organ, generating bioactive metabolites, enzymes or small molecules that can impact host physiology. Gut dysbacteriosis is associated with many intestinal diseases including (but not limited to) inflammatory bowel disease, primary sclerosing cholangitis‐IBD, irritable bowel syndrome, chronic constipation, osmotic diarrhoea and colorectal cancer. The potential pathogenic mechanism of gut dysbacteriosis associated with intestinal diseases includes the alteration of composition of gut microbiota as well as the gut microbiota–derived signalling molecules. The many correlations between the latter and the susceptibility for intestinal diseases has placed a spotlight on the gut microbiome as a potential novel target for therapeutics. Currently, faecal microbial transplantation, dietary interventions, use of probiotics, prebiotics and drugs are the major therapeutic tools utilized to impact dysbacteriosis and associated intestinal diseases. In this review, we systematically summarized the role of intestinal microbiome in the occurrence and development of intestinal diseases. The potential mechanism of the complex interplay between gut dysbacteriosis and intestinal diseases, and the treatment methods are also highlighted.

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Environmental-mediated intestinal homeostasis in neonatal mice

Cited by 14 publications

References 30 publications

Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function

Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function

The Role of the Microbiome in Food Allergy: A Review

Gut dysbacteriosis and intestinal disease: mechanism and treatment

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