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However, the players and mechanisms that underlie protease regulation in the intestinal lumen have remained unclear. Here we show that\n                    <jats:italic>Paraprevotella<\/jats:italic>\n                    strains isolated from the faecal microbiome of healthy human donors are potent trypsin-degrading commensals. Mechanistically,\n                    <jats:italic>Paraprevotella<\/jats:italic>\n                    recruit trypsin to the bacterial surface through type IX secretion system-dependent polysaccharide-anchoring proteins to promote trypsin autolysis.\n                    <jats:italic>Paraprevotella<\/jats:italic>\n                    colonization protects IgA from trypsin degradation and enhances the effectiveness of oral vaccines against\n                    <jats:italic>Citrobacter rodentium<\/jats:italic>\n                    . Moreover,\n                    <jats:italic>Paraprevotella<\/jats:italic>\n                    colonization inhibits lethal infection with murine hepatitis virus-2, a mouse coronavirus that is dependent on trypsin and trypsin-like proteases for entry into host cells\n                    <jats:sup>4,5<\/jats:sup>\n                    . Consistently, carriage of putative genes involved in trypsin degradation in the gut microbiome was associated with reduced severity of diarrhoea in patients with SARS-CoV-2 infection. Thus, trypsin-degrading commensal colonization may contribute to the maintenance of intestinal homeostasis and protection from pathogen infection.\n                  <\/jats:p>","DOI":"10.1038\/s41586-022-05181-3","type":"journal-article","created":{"date-parts":[[2022,9,7]],"date-time":"2022-09-07T12:03:47Z","timestamp":1662552227000},"page":"582-589","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":110,"title":["Identification of trypsin-degrading commensals in the large 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