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Review
. 2017 Feb;17(1):48-59.
doi: 10.4110/in.2017.17.1.48. Epub 2017 Feb 23.

Beyond Hygiene: Commensal Microbiota and Allergic Diseases

Affiliations
Review

Beyond Hygiene: Commensal Microbiota and Allergic Diseases

Sung-Wook Hong et al. Immune Netw. 2017 Feb.

Abstract

Complex communities of microorganisms, termed commensal microbiota, inhabit mucosal surfaces and profoundly influence host physiology as well as occurrence of allergic diseases. Perturbing factors such as the mode of delivery, dietary fibers and antibiotics can influence allergic diseases by altering commensal microbiota in affected tissues as well as in intestine. Here, we review current findings on the relationship between commensal microbiota and allergic diseases, and discuss the underlying mechanisms that contribute to the regulation of allergic responses by commensal microbiota.

Keywords: Asthma; Atopic dermatitis; Commensal microbiota; Food allergy.

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Conflict of interest statement

CONFLICTS OF INTEREST: The authors have no financial conflict of interest.

Figures

Figure 1
Figure 1. Differences between microbial communities based on anatomic sites and factors influencing dysbiosis of commensal microbiota. (A) Each mucosal site harbors distinct microbial community as indicated by principal coordinates plot (reproduced from (4)). Microbial populations within skin are more variable than those at other mucosal sites. Inhabitants within nasal cavity resembles those in skin. Lung microbiota was reported to be similar with those in oral cavity. (B) Several factors can cause perturbations of commensal microbiota, leading to the states of microbial dysbiosis, which is associated with allergic diseases.
Figure 2
Figure 2. Interplay between intestinal microbiota and immune cells in the context of IgE-mediated food allergy. pTreg cells are abundant in the small intestine. Dietary antigens- or intestinal microbes-induced pTreg cells, distinguished from each other by RORγt expression, can suppress mucosal TH2 cells generated against food allergens. TH2 cells can induce IgE-producing plasma cells and increase mucosal mast cells expressing IL-9 or mediating food allergic symptoms through the degranulation of histamine, PAF and so on. IL-13 or IL-9 can increase intestinal permeability to food allergens, while SCFAs or IL-22 induced by intestinal microbiota in colon can promote intestinal barrier functions. Certain species of intestinal microbiota such as Bifidobacterium can induce apoptosis of mast cells, thus preventing food allergy.

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