Influences on allergic mechanisms through gut, lung, and skin microbiome exposures
Andrea M. Kemter, Cathryn R. Nagler
Andrea M. Kemter, Cathryn R. Nagler
Published February 25, 2019
Citation Information: J Clin Invest. 2019;129(4):1483-1492. https://doi.org/10.1172/JCI124610.
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Review Series

Influences on allergic mechanisms through gut, lung, and skin microbiome exposures

Abstract

In industrialized societies the incidence of allergic diseases like atopic dermatitis, food allergies, and asthma has risen alarmingly over the last few decades. This increase has been attributed, in part, to lifestyle changes that alter the composition and function of the microbes that colonize the skin and mucosal surfaces. Strategies that reverse these changes to establish and maintain a healthy microbiome show promise for the prevention and treatment of allergic disease. In this Review, we will discuss evidence from preclinical and clinical studies that gives insights into how the microbiota of skin, intestinal tract, and airways influence immune responses in the context of allergic sensitization.

Authors

Andrea M. Kemter, Cathryn R. Nagler

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Figure 1

Skin commensals and an intact skin barrier promote tolerance induction, while skin barrier impairment and dysbiosis can drive type 2 inflammation.

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Skin commensals and an intact skin barrier promote tolerance induction, ...
(A) In healthy individuals, the skin is colonized with a variety of skin commensals. Their composition depends on the local microenvironment and is balanced by antimicrobial peptides and lipids produced by the host or the commensals themselves. They also protect the host from colonization with potentially pathogenic bacteria. Colonization with beneficial commensals further induces local immune responses that protect the host from pathogens and promote induction of tolerance to environmental antigens. (B) Impaired skin barrier function is one of the main predisposing factors for atopic dermatitis (AD) development. Loss of microbial diversity as well as an overabundance of Staphylococcus aureus is also a common phenomenon on lesional skin of AD patients. Potentially pathogenic S. aureus strains can produce a number of molecules aiding in penetration of the host skin and driving type 2 immune responses, thereby exacerbating AD. Environmental antigens taken up through the inflamed skin are encountered in a pro–type 2 environment, which can lead to allergic sensitization with production of antigen-specific IgE. AMP, antimicrobial peptide; APC, antigen-presenting cell; LN, lymph node; SEB, staphylococcal enterotoxin B; Teff, effector T cell; Treg, regulatory T cell; TSLP, thymic stromal lymphopoietin.