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Gut microbiota and Hashimoto's thyroiditis.
Rev Endocr Metab Disord. 2018 Dec; 19(4):293-300.RE

Abstract

About two third of the human microbial commensal community, namely the gut microbiota, is hosted by the gastrointestinal tract which represents the largest interface of the organism to the external environment. This microbial community co-evolved in a symbiotic relationship with the human beings. Growing evidence support the notion that the microbiota plays a significant role in maintaining nutritional, metabolic and immunologic homeostasis in the host. Microbiota, beside the expected role in maintaining gastrointestinal homeostasis also exerts metabolic functions in nutrients digestion and absorption, detoxification and vitamins' synthesis. Intestinal microbiota is also key in the correct development of the lymphoid system, 70% of which resides at the intestinal level. Available studies, both in murine models and humans, have shown an altered ratio between the different phyla, which characterize a" normal" gut microbiota, in a number of different disorders including obesity, to which a significant part of the studies on intestinal microbiota has been addressed so far. These variations in gut microbiota composition, known as dysbiosis, has been also described in patients bearing intestinal autoimmune diseases as well as type 1 diabetes mellitus, systemic sclerosis and systemic lupus erythematosus. Being Hashimoto's thyroiditis the most frequent autoimmune disorder worldwide, the analysis of the reciprocal influence with intestinal microbiota gained interest. The whole thyroid peripheral homeostasis may be sensitive to microbiota changes but there is also evidence that the genesis and progression of autoimmune thyroid disorders may be significantly affected from a changing intestinal microbial composition or even from overt dysbiosis. In this brief review, we focused on the main features which characterize the reciprocal influence between microbiota and thyroid autoimmunity described in the most recent literature.

Authors+Show Affiliations

Endocrinology Section, Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome, Latina, Italy. camilla.virili@uniroma1.it. Endocrinology Unit, Santa Maria Goretti Hospital, Latina, Italy. camilla.virili@uniroma1.it.Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, I-56126, Pisa, Italy.Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.Interdepartmental Program of Molecular & Clinical Endocrinology, and Women's Endocrine Health, University Hospital "G. Martino", Messina, Italy. Department of Clinical and Experimental Medicine, University of Messina, Policlinico Universitario G. Martino, Messina, Italy.Endocrinology Section, Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome, Latina, Italy. Endocrinology Unit, Santa Maria Goretti Hospital, Latina, Italy.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

30294759

Citation

Virili, Camilla, et al. "Gut Microbiota and Hashimoto's Thyroiditis." Reviews in Endocrine & Metabolic Disorders, vol. 19, no. 4, 2018, pp. 293-300.
Virili C, Fallahi P, Antonelli A, et al. Gut microbiota and Hashimoto's thyroiditis. Rev Endocr Metab Disord. 2018;19(4):293-300.
Virili, C., Fallahi, P., Antonelli, A., Benvenga, S., & Centanni, M. (2018). Gut microbiota and Hashimoto's thyroiditis. Reviews in Endocrine & Metabolic Disorders, 19(4), 293-300. https://doi.org/10.1007/s11154-018-9467-y
Virili C, et al. Gut Microbiota and Hashimoto's Thyroiditis. Rev Endocr Metab Disord. 2018;19(4):293-300. PubMed PMID: 30294759.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gut microbiota and Hashimoto's thyroiditis. AU - Virili,Camilla, AU - Fallahi,Poupak, AU - Antonelli,Alessandro, AU - Benvenga,Salvatore, AU - Centanni,Marco, PY - 2018/10/9/pubmed PY - 2019/4/11/medline PY - 2018/10/9/entrez KW - Dysbiosis KW - Hashimoto’s thyroiditis KW - Microbiota KW - Probiotic KW - Thyroid autoimmunity SP - 293 EP - 300 JF - Reviews in endocrine & metabolic disorders JO - Rev Endocr Metab Disord VL - 19 IS - 4 N2 - About two third of the human microbial commensal community, namely the gut microbiota, is hosted by the gastrointestinal tract which represents the largest interface of the organism to the external environment. This microbial community co-evolved in a symbiotic relationship with the human beings. Growing evidence support the notion that the microbiota plays a significant role in maintaining nutritional, metabolic and immunologic homeostasis in the host. Microbiota, beside the expected role in maintaining gastrointestinal homeostasis also exerts metabolic functions in nutrients digestion and absorption, detoxification and vitamins' synthesis. Intestinal microbiota is also key in the correct development of the lymphoid system, 70% of which resides at the intestinal level. Available studies, both in murine models and humans, have shown an altered ratio between the different phyla, which characterize a" normal" gut microbiota, in a number of different disorders including obesity, to which a significant part of the studies on intestinal microbiota has been addressed so far. These variations in gut microbiota composition, known as dysbiosis, has been also described in patients bearing intestinal autoimmune diseases as well as type 1 diabetes mellitus, systemic sclerosis and systemic lupus erythematosus. Being Hashimoto's thyroiditis the most frequent autoimmune disorder worldwide, the analysis of the reciprocal influence with intestinal microbiota gained interest. The whole thyroid peripheral homeostasis may be sensitive to microbiota changes but there is also evidence that the genesis and progression of autoimmune thyroid disorders may be significantly affected from a changing intestinal microbial composition or even from overt dysbiosis. In this brief review, we focused on the main features which characterize the reciprocal influence between microbiota and thyroid autoimmunity described in the most recent literature. SN - 1573-2606 UR - https://www.unboundmedicine.com/medline/citation/30294759/full_citation DB - PRIME DP - Unbound Medicine ER -