Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Jul 17:9:1584.
doi: 10.3389/fimmu.2018.01584. eCollection 2018.

Microbiome and Allergic Diseases

Affiliations
Review

Microbiome and Allergic Diseases

Mariona Pascal et al. Front Immunol. .

Abstract

Allergic diseases, such as respiratory, cutaneous, and food allergy, have dramatically increased in prevalence over the last few decades. Recent research points to a central role of the microbiome, which is highly influenced by multiple environmental and dietary factors. It is well established that the microbiome can modulate the immune response, from cellular development to organ and tissue formation exerting its effects through multiple interactions with both the innate and acquired branches of the immune system. It has been described at some extent changes in environment and nutrition produce dysbiosis in the gut but also in the skin, and lung microbiome, inducing qualitative and quantitative changes in composition and metabolic activity. Here, we review the potential role of the skin, respiratory, and gastrointestinal tract (GIT) microbiomes in allergic diseases. In the GIT, the microbiome has been proven to be important in developing either effector or tolerant responses to different antigens by balancing the activities of Th1 and Th2 cells. In the lung, the microbiome may play a role in driving asthma endotype polarization, by adjusting the balance between Th2 and Th17 patterns. Bacterial dysbiosis is associated with chronic inflammatory disorders of the skin, such as atopic dermatitis and psoriasis. Thus, the microbiome can be considered a therapeutical target for treating inflammatory diseases, such as allergy. Despite some limitations, interventions with probiotics, prebiotics, and/or synbiotics seem promising for the development of a preventive therapy by restoring altered microbiome functionality, or as an adjuvant in specific immunotherapy.

Keywords: allergic diseases; allergy; microbiome; microbiota; prebiotics; probiotics; synbiotics.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Interaction between gut microbiota and immune system. Gut microbiota metabolites and dietary factors constitute the main antigen load of the gastrointestinal tract. Macrophages (CXCR1+) and dendritic cells (DCs) are stimulated and T regulatory (Treg) cells are activated by metabolic products such as short chain fatty acid (SCFA). Follicular T cells activate B cells inducing the production of IgA antibodies.
Figure 2
Figure 2
Dysbiosis induce qualitative and quantitative changes in the microbiota that directly affect immunological mechanisms leading to allergic diseases.

References

    1. Akdis CA. Allergy and hypersensitivity: mechanisms of allergic disease. Curr Opin Immunol (2006) 18(6):718–26. 10.1016/j.coi.2006.09.016 - DOI - PubMed
    1. Veldhoen M, Uyttenhove C, van Snick J, Helmby H, Westendorf A, Buer J, et al. Transforming growth factor-beta ‘reprograms’ the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset. Nat Immunol (2008) 9(12):1341–6. 10.1038/ni.1659 - DOI - PubMed
    1. Akinbami LJ, Simon AE, Rossen LM. Changing trends in asthma prevalence among children. Pediatrics (2016) 137(1). 10.1542/peds.2015-2354 - DOI - PMC - PubMed
    1. Prescott SL, Pawankar R, Allen KJ, Campbell DE, Sinn J, Fiocchi A, et al. A global survey of changing patterns of food allergy burden in children. World Allergy Organ J (2013) 6(1):21. 10.1186/1939-4551-6-21 - DOI - PMC - PubMed
    1. Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin North Am (2015) 35(1):45–59. 10.1016/j.iac.2014.09.004 - DOI - PMC - PubMed