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Журнал микробиологии, эпидемиологии и иммунобиологии. 2021; 98: 221-230

Нарушения кишечной микробиоты при расстройствах аутистического спектра: новые горизонты в поиске патогенетических подходов к терапии. Часть 2. Ось кишечник–мозг в патогенезе расстройств аутистического спектра

Благонравова А. С., Жиляева Т. В., Квашнина Д. В.

https://doi.org/10.36233/0372-9311-83

Аннотация

Вторая часть обзора литературы, посвящённого роли нарушений кишечной микробиоты в патогенезе расстройств аутистического спектра (РАС), содержит анализ опубликованной литературы о возможных механизмах влияния дисбиоза кишечника на функцию центральной нервной системы и симптомы РАС и, наоборот, влияния нервной системы на кишечную микробиоту. Рассмотрены гипотезы медленного воспаления, гиперсеротонинемии, продукции токсичных метаболитов кишечной микробиотой, нарушения проницаемости кишечной стенки, а также влияния дисбиоза кишечника на синтез аминокислот, витаминов и других биологически активных веществ, потенциально задействованных в этиологии и патогенезе РАС. Приведены экспериментальные и клинические данные в поддержку перечисленных гипотез. Сформулированы основные механизмы оси кишечник–мозг, которые могут иметь отношение к патогенезу РАС.

Список литературы

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Journal of microbiology, epidemiology and immunobiology. 2021; 98: 221-230

Dysbiosis of intestinal microbiota in autism spectrum disorders: new horizons in search for pathogenetic approaches to therapy. Part 2. Gut–brain axis in pathogenesis of autism spectrum disorders

Blagonravova A. S., Zhilyaeva T. V., Kvashnina D. V.

https://doi.org/10.36233/0372-9311-83

Abstract

The second part of the literature review on the role of intestinal microbiota disturbances in the pathogenesis of autism spectrum disorders (ASD) is devoted to the analysis of published literature on the possible mechanisms underlying the impact of intestinal dysbiosis on the function of the central nervous system and symptoms of ASD and vice versa, the effect of the nervous system on the intestinal microbiota. The hypotheses of slow inflammation, hyperserotoninemia, the production of toxic metabolites of the intestinal microbiota, impaired intestinal wall permeability, and the effect of intestinal dysbiosis on the synthesis of amino acids, vitamins and other biologically active substances that are potentially involved in the etiology and pathogenesis of ASD are considered. Available to date experimental and clinical data supporting these hypotheses are presented. The main mechanisms of the so-called gut-brain axis, which may be related to the pathogenesis of ASD, are formulated.

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