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Studies in animal models of Gulf War Syndrome suggest gut-microbial dysbiosis likely increases immune activation mediated by the TLR4-S100/RAGE-iNOS pathway of EGCs followed by redox instability and dysfunction of the GI barrier (Kimono et al., 2019), further implicating the microbiota as an important regulator of enteric neuronal and glial physiology, independent of CNS modulation

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