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It is argued that gut dysbiosis, a central feature of IBD, is a fundamental trigger that, through a compromised gut barrier, drives systemic inflammation and, subsequently, neuroinflammation

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PrfA is activated upon entry into the cytosol via allosteric regulation by glutathione, however PrfA* mutations such as the G145S mutation result in constitutive virulence gene expression and upregulation of uhpT, the L