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. 2021 Apr 22;11:615075. doi: 10.3389/fcimb.2021.615075

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Copyright © 2021 Huang, Liao, Liu, Zhong, Cai and Long

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The possible mechanisms of Parkinson’s disease caused by intestinal dysbiosis. The increased intestinal permeability: The decrease of SCFAs concentration in intestinal cavity leads to local inflammation, and also affects the expression of tight junction proteins, including claudin 1 and claudin 2. The increased BBB permeability: Intestinal dysbiosis leads to decreased claudin expression. Inflammation and oxidative stress: The decrease of SCFAs concentration leads to the dysfunction of microglia; the increase of LPS concentration activates microglia, NLRP3 inflammasome and promotes the expression of iNOS. Changes of the production of dopamine: Dysbiosis changes the level of dopamine produced in the gut; the concentration of SCFAs affects the secretion of ghrelin, thus affecting the secretion of dopamine in substantia nigra. Molecular mimicry: Bacterial amyloids may induce immune response to αSyn in human body. SCFAs, short-chain fatty acids; BBB, blood–brain–barrier; LPS, lipopolysaccharide; iNOS, inducible NO synthase.