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. 2023 Jul 27;14:1219942. doi: 10.3389/fmicb.2023.1219942

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Copyright © 2023 Zhao, Hu, Zhou, Yang, Shen, You and Xue.

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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Respiratory tract infections can alter the microecology of the intestines, leading to changes in the abundance of gut microbiome and a reduction in bacteria that produce short-chain fatty acids (SCFAs). So there is a decrease in SCFA production. The reduction in SCFA levels can impact the function and fate of various immune cells, including dendritic cells (DCs), regulatory T cells (Tregs), eosinophils, and type 2 innate lymphoid cells (ILC2s). Additionally, the SCFA receptor GPR43 can interact with the NOD-like receptor protein 3 (NLRP3) to promote the aggregation and signal transduction of the mitochondrial antiviral signaling protein MAVS. When acetate binds to GPR43, it enhances MAVS aggregation, activates downstream TBK1/IRF3, and promotes the production of interferon-I (IFN-I). IFN-I can increase the number of Th2 cells and eosinophils, which can lead to airway hyperresponsiveness in asthma.