Inflammation: a highly conserved, Janus-like phenomenon—a gastroenterologist’ perspective

Inflammation is the result of the loss of host’s resilience towards the surrounding world. at gross tissue level, inflammation coincides with fluid leakage from vessels, swelling, and blood stasis and extravasation of mononuclear/macrophage cells. biochemically, these events lead to anoxia and dramatic changes: interruption of the mitochondrial oxidative phosphorylation, influx of the m1 macrophage subset, which live on anaerobic glycolysis. fall of atp then leads to energy shortage and debt. in their chronic forms, these phenomena are now known to mark a number of degenerative disorders that have invaded the western world since the last century: parkinson’s disease, alzheimer’s syndromes, rheumatic diseases, metabolic diseases. intriguingly, these affections seem to derive from the gut, along two possible pathways. a sort of ascending loss of function caused by accumulation of (and hyperreactivity to) proteins released to restrain spread of enteric viruses: the alpha-synucleins, now increasingly spotted in relation to parkinson’s pathogenesis. the second pathway would entail the intellectual decline perhaps brought about by large use of food containing the proteins of red processed meat. the bacterium bilophila wadsworthia, thriving in this meat, can erode the mucus layer on colon surfaces, allowing further bacterial flora to approach lining cells, so upgrading the alarm state. we discuss two strategies to prevent such instability from ending up to full-blown inflammatory bowel disease: physical exercise and systematic switch to fibre-containing diets.