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It highlights the pathological processes through which gut microbiota dysbiosis exacerbates systemic inflammation and lung injury via multiple pathways, including alterations in metabolites (such as bile acids and tryptophan), inhibition of the anti-inflammatory pathway mediated by the vagus nerve, and activation of TLR signals in the lungs by circulating toxins

A phylogenetic study (47) highlighted that ChaC2 evolved earlier than ChaC1 and shares key structural similarities with ChaC proteins of lower eukaryotes

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The interactions between toxic gluten peptides and specific cells in lamina propria such as epithelial cells, macrophages and dendritic cells induce an innate immune response by up-regulating the expression of different mediators such as interleukin 15 (IL-15) with subsequent massive increase of intraepithelial lymphocytes [22]