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High salt diet stimulates gut Th17 response and exacerbates TNBS-induced colitis in mice

Those of ordinary skill in the art are able to determine the mucoadhesive characteristics of the compositions provided herein, and thus determine appropriate ranges

The picture that emerges from these experiments is that endogenous GSH is not just an inhibitor of inflammation, but it is required to allow a proper response to infection, and direct the migration of inflammatory PMN away from the lung, where they cause ARDS, and towards the site of infection, where they kill bacteria (Figure 6)