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It provides favorable structure to bakery products but unfortunately causes disease conditions with increasing prevalence. In the human gastrointestinal tract, gluten is cleaved into proline and gluten rich peptides that are not degraded further. These peptides trigger immune responses that might lead to celiac disease, wheat allergy, and non-celiac gluten sensitivity. The main treatment option is a gluten-free diet. Alternatively, using enzymes or microorganisms with gluten-degrading properties might alleviate the disease. These components can be used during food production or could be introduced into the digestive tract as food supplements. In addition, natural food from the environment is known to enrich the microbial communities in gut and natural environmental microbial communities have high potential to degrade gluten. It remains to be investigated if food and environment-induced changes in the gut microbiome could contribute to the triggering of gluten-related diseases.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Key points<\/jats:title>\n                <jats:p>\u2022 <jats:italic>Wheat proteins, gluten, are incompletely digested in human digestive tract leading to gluten intolerance.<\/jats:italic><\/jats:p>\n                <jats:p>\u2022 <jats:italic>The only efficient treatment of gluten intolerance is life-long gluten-free diet.<\/jats:italic><\/jats:p>\n                <jats:p>\u2022 <jats:italic>Environmental bacteria acquired together with food could be source of gluten-degrading bacteria detoxifying undigested gluten peptides.<\/jats:italic><\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00253-021-11263-5","type":"journal-article","created":{"date-parts":[[2021,4,10]],"date-time":"2021-04-10T13:02:41Z","timestamp":1618059761000},"page":"3045-3059","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Gluten-degrading bacteria: availability and applications"],"prefix":"10.1007","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9044-0971","authenticated-orcid":false,"given":"Viia","family":"K\u00f5iv","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0260-3601","authenticated-orcid":false,"given":"Tanel","family":"Tenson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,4,10]]},"reference":[{"key":"11263_CR1","doi-asserted-by":"publisher","first-page":"5721","DOI":"10.1128\/JCM.43.11.5721-5732.2005","volume":"43","author":"JA Aas","year":"2005","unstructured":"Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE (2005) Defining the normal bacterial flora of the oral cavity. 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