Metabolites of microbiota response to tryptophan and intestinal mucosal immunity: A therapeutic target to control intestinal inflammation.
Identifieur interne : 000115 ( Main/Exploration ); précédent : 000114; suivant : 000116Metabolites of microbiota response to tryptophan and intestinal mucosal immunity: A therapeutic target to control intestinal inflammation.
Auteurs : Jie Zhang [République populaire de Chine] ; Shengwei Zhu [République populaire de Chine] ; Ning Ma [République populaire de Chine] ; Lee J. Johnston [États-Unis] ; Chaodong Wu [États-Unis] ; Xi Ma [République populaire de Chine]Source :
- Medicinal research reviews [ 1098-1128 ] ; 2020.
Abstract
In a complex, diverse intestinal environment, commensal microbiota metabolizes excessive dietary tryptophan to produce more bioactive metabolites connecting with kinds of diverse process, such as host physiological defense, homeostasis, excessive immune activation and the progression and outcome of different diseases, such as inflammatory bowel disease, irritable bowel syndrome and others. Although commensal microbiota includes bacteria, fungi, and protozoa and all that, they often have the similar metabolites in tryptophan metabolism process via same or different pathways. These metabolites can work as signal to activate the innate immunity of intestinal mucosa and induce the rapid inflammation response. They are critical in reconstruction of lumen homeostasis as well. This review aims to seek the potential function and mechanism of microbiota-derived tryptophan metabolites as targets to regulate and shape intestinal immune function, which mainly focused on two aspects. First, analyze the character of tryptophan metabolism in bacteria, fungi, and protozoa, and assess the functions of their metabolites (including indole and eight other derivatives, serotonin (5-HT) and d-tryptophan) on regulating the integrity of intestinal epithelium and the immunity of the intestinal mucosa. Second, focus on the mediator and pathway for their recognition, transfer and crosstalk between microbiota-derived tryptophan metabolites and intestinal mucosal immunity. Disruption of intestinal homeostasis has been described in different intestinal inflammatory diseases, available data suggest the remarkable potential of tryptophan-derived aryl hydrocarbon receptor agonists, indole derivatives on lumen equilibrium. These metabolites as preventive and therapeutic interventions have potential to promote proinflammatory or anti-inflammatory responses of the gut.
DOI: 10.1002/med.21752
PubMed: 33174230
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Johnston</name><affiliation wicri:level="2"><nlm:affiliation>West Central Research and Outreach Center, University of Minnesota, Morris, Minnesota, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>West Central Research and Outreach Center, University of Minnesota, Morris, Minnesota</wicri:regionArea><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Wu, Chaodong" sort="Wu, Chaodong" uniqKey="Wu C" first="Chaodong" last="Wu">Chaodong Wu</name><affiliation wicri:level="2"><nlm:affiliation>Department of Nutrition and Food Science, Texas A&M University, College Station, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Nutrition and Food Science, Texas A&M University, College Station, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Ma, Xi" sort="Ma, Xi" uniqKey="Ma X" first="Xi" last="Ma">Xi Ma</name><affiliation wicri:level="3"><nlm:affiliation>State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Medicinal research reviews</title><idno type="eISSN">1098-1128</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In a complex, diverse intestinal environment, commensal microbiota metabolizes excessive dietary tryptophan to produce more bioactive metabolites connecting with kinds of diverse process, such as host physiological defense, homeostasis, excessive immune activation and the progression and outcome of different diseases, such as inflammatory bowel disease, irritable bowel syndrome and others. Although commensal microbiota includes bacteria, fungi, and protozoa and all that, they often have the similar metabolites in tryptophan metabolism process via same or different pathways. These metabolites can work as signal to activate the innate immunity of intestinal mucosa and induce the rapid inflammation response. They are critical in reconstruction of lumen homeostasis as well. This review aims to seek the potential function and mechanism of microbiota-derived tryptophan metabolites as targets to regulate and shape intestinal immune function, which mainly focused on two aspects. First, analyze the character of tryptophan metabolism in bacteria, fungi, and protozoa, and assess the functions of their metabolites (including indole and eight other derivatives, serotonin (5-HT) and d-tryptophan) on regulating the integrity of intestinal epithelium and the immunity of the intestinal mucosa. Second, focus on the mediator and pathway for their recognition, transfer and crosstalk between microbiota-derived tryptophan metabolites and intestinal mucosal immunity. Disruption of intestinal homeostasis has been described in different intestinal inflammatory diseases, available data suggest the remarkable potential of tryptophan-derived aryl hydrocarbon receptor agonists, indole derivatives on lumen equilibrium. These metabolites as preventive and therapeutic interventions have potential to promote proinflammatory or anti-inflammatory responses of the gut.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">33174230</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-1128</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Nov</Month><Day>10</Day></PubDate></JournalIssue><Title>Medicinal research reviews</Title><ISOAbbreviation>Med Res Rev</ISOAbbreviation></Journal><ArticleTitle>Metabolites of microbiota response to tryptophan and intestinal mucosal immunity: A therapeutic target to control intestinal inflammation.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/med.21752</ELocationID><Abstract><AbstractText>In a complex, diverse intestinal environment, commensal microbiota metabolizes excessive dietary tryptophan to produce more bioactive metabolites connecting with kinds of diverse process, such as host physiological defense, homeostasis, excessive immune activation and the progression and outcome of different diseases, such as inflammatory bowel disease, irritable bowel syndrome and others. Although commensal microbiota includes bacteria, fungi, and protozoa and all that, they often have the similar metabolites in tryptophan metabolism process via same or different pathways. These metabolites can work as signal to activate the innate immunity of intestinal mucosa and induce the rapid inflammation response. They are critical in reconstruction of lumen homeostasis as well. This review aims to seek the potential function and mechanism of microbiota-derived tryptophan metabolites as targets to regulate and shape intestinal immune function, which mainly focused on two aspects. First, analyze the character of tryptophan metabolism in bacteria, fungi, and protozoa, and assess the functions of their metabolites (including indole and eight other derivatives, serotonin (5-HT) and d-tryptophan) on regulating the integrity of intestinal epithelium and the immunity of the intestinal mucosa. Second, focus on the mediator and pathway for their recognition, transfer and crosstalk between microbiota-derived tryptophan metabolites and intestinal mucosal immunity. Disruption of intestinal homeostasis has been described in different intestinal inflammatory diseases, available data suggest the remarkable potential of tryptophan-derived aryl hydrocarbon receptor agonists, indole derivatives on lumen equilibrium. These metabolites as preventive and therapeutic interventions have potential to promote proinflammatory or anti-inflammatory responses of the gut.</AbstractText><CopyrightInformation>© 2020 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><Identifier Source="ORCID">https://orcid.org/0000-0001-5010-0833</Identifier><AffiliationInfo><Affiliation>State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Animal Husbandry and Veterinary Department, Beijing Vocational College of Agriculture, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Shengwei</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Botany, Key laboratory of plant molecular physiology, Chinese Academy of Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Ning</ForeName><Initials>N</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-6473-595X</Identifier><AffiliationInfo><Affiliation>State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnston</LastName><ForeName>Lee J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>West Central Research and Outreach Center, University of Minnesota, Morris, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Chaodong</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Nutrition and Food Science, Texas A&M University, College Station, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Xi</ForeName><Initials>X</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-4562-9331</Identifier><AffiliationInfo><Affiliation>State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2018YFD0500601 and 2017YFD0500501</GrantID><Agency>National Key R&D Program of China</Agency><Country></Country></Grant><Grant><GrantID>31930106</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant><Grant><GrantID>31829004</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant><Grant><GrantID>31722054</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>11</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Med Res Rev</MedlineTA><NlmUniqueID>8103150</NlmUniqueID><ISSNLinking>0198-6325</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">intestinal inflammatory diseases</Keyword><Keyword MajorTopicYN="N">microbes</Keyword><Keyword MajorTopicYN="N">mucosal immunity</Keyword><Keyword MajorTopicYN="N">tryptophan metabolites</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>05</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>10</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>11</Month><Day>11</Day><Hour>6</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>11</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33174230</ArticleId><ArticleId IdType="doi">10.1002/med.21752</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Ma N, Guo P, Zhang J, et al. 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Johnston</name></region><name sortKey="Wu, Chaodong" sort="Wu, Chaodong" uniqKey="Wu C" first="Chaodong" last="Wu">Chaodong Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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