Microbiome and asthma
- PMID: 29318023
- PMCID: PMC5755449
- DOI: 10.1186/s40733-017-0037-y
Microbiome and asthma
Abstract
The mucosal immune system is in constant communication with the vast diversity of microbes present on body surfaces. The discovery of novel molecular mechanisms, which mediate host-microbe communication, have highlighted the important roles played by microbes in influencing mucosal immune responses. Dendritic cells, epithelial cells, ILCs, T regulatory cells, effector lymphocytes, NKT cells and B cells can all be influenced by the microbiome. Many of the mechanisms being described are bacterial strain- or metabolite-specific. Microbial dysbiosis in the gut and the lung is increasingly being associated with the incidence and severity of asthma. More accurate endotyping of patients with asthma may be assisted by further analysis of the composition and metabolic activity of an individual's microbiome. In addition, the efficacy of specific therapeutics may be influenced by the microbiome and novel bacterial-based therapeutics should be considered in future clinical studies.
Keywords: Asthma; Bacteria; Histamine; Immune tolerance; Microbiome; Mucosal immune system; Short-chain fatty acids.
Conflict of interest statement
Not applicableNot applicableLOM is a consultant to Alimentary Health Ltd. and has received research funding from GlaxoSmithKline. CA has received research support from Novartis and Stallergenes and consulted for Actellion, Aventis and Allergopharma. MS, RF and NL have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
-
- Huang Y, Marsland B, Bunyavanich S, O'Mahony L, Leung D, Muraro A, et al. (2017). The microbiome in allergic disease: current understanding and future opportunities—2017 PRACTALL document of the American Academy of Allergy, Asthma & Immunology and the European academy of allergy and clinical immunology. J Allergy Clin Immunol. 2017;139:1099–1110. doi: 10.1016/j.jaci.2017.02.007. - DOI - PMC - PubMed
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