Fecal microbiota transplantation (FMT) could reverse the severity of experimental necrotizing enterocolitis (NEC) via oxidative stress modulation.
Identifieur interne : 000368 ( Main/Exploration ); précédent : 000367; suivant : 000369Fecal microbiota transplantation (FMT) could reverse the severity of experimental necrotizing enterocolitis (NEC) via oxidative stress modulation.
Auteurs : Xiaomei Li [République populaire de Chine] ; Xiaowen Li [République populaire de Chine] ; Qingjuan Shang [République populaire de Chine] ; Zongwei Gao [République populaire de Chine] ; Fabao Hao [République populaire de Chine] ; Hongjie Guo [République populaire de Chine] ; Chunbao Guo [République populaire de Chine]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Entérocolite nécrosante (immunologie), Entérocolite nécrosante (thérapie), Espèces réactives de l'oxygène (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Inflammation (immunologie), Microbiome gastro-intestinal (immunologie), Modèles animaux (MeSH), Muqueuse intestinale (immunologie), Nitric oxide synthase type III (métabolisme), Récepteur de type Toll-4 (métabolisme), Récepteur-9 de type Toll-like (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Stress oxydatif (MeSH), Transcytose (MeSH), Transduction du signal (MeSH), Transplantation de microbiote fécal (MeSH), Évolution de la maladie (MeSH).
- MESH :
- génétique : Glutarédoxines.
- immunologie : Entérocolite nécrosante, Inflammation, Microbiome gastro-intestinal, Muqueuse intestinale.
- métabolisme : Espèces réactives de l'oxygène, Glutarédoxines, Nitric oxide synthase type III, Récepteur de type Toll-4, Récepteur-9 de type Toll-like.
- thérapie : Entérocolite nécrosante.
- Animaux, Humains, Modèles animaux, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif, Transcytose, Transduction du signal, Transplantation de microbiote fécal, Évolution de la maladie.
English descriptors
- KwdEn :
- Animals (MeSH), Disease Progression (MeSH), Enterocolitis, Necrotizing (immunology), Enterocolitis, Necrotizing (therapy), Fecal Microbiota Transplantation (MeSH), Gastrointestinal Microbiome (immunology), Glutaredoxins (genetics), Glutaredoxins (metabolism), Humans (MeSH), Inflammation (immunology), Intestinal Mucosa (immunology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Models, Animal (MeSH), Nitric Oxide Synthase Type III (metabolism), Oxidative Stress (MeSH), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH), Toll-Like Receptor 4 (metabolism), Toll-Like Receptor 9 (metabolism), Transcytosis (MeSH).
- MESH :
- chemical , genetics : Glutaredoxins.
- immunology : Enterocolitis, Necrotizing, Gastrointestinal Microbiome, Inflammation, Intestinal Mucosa.
- chemical , metabolism : Glutaredoxins, Nitric Oxide Synthase Type III, Reactive Oxygen Species, Toll-Like Receptor 4, Toll-Like Receptor 9.
- therapy : Enterocolitis, Necrotizing.
- Animals, Disease Progression, Fecal Microbiota Transplantation, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Animal, Oxidative Stress, Signal Transduction, Transcytosis.
Abstract
Fecal microbiota transplantation (FMT) has been used successfully to treat a variety of gastroenterological diseases. The alterations of microbiota in mouse models of necrotizing enterocolitis (NEC) as well as in patients suggested the possibility of treating NEC with FMT. Here we show that FMT caused an improvement in the histopathology and symptoms of NEC in WT mice, but not Grx1-/- mice. FMT eliminated O2•- production and promoted NO production in experimental NEC mice though the modulation of S-glutathionylation of eNOS (eNOS-SSG). FMT decreased the extent of TLR4-mediated proinflammatory signaling though TLR9 in the intestinal mucosa tissue. FMT also suppressed intestinal apoptosis and bacterial translocation across the intestinal barrier, which was accompanied by decreased inflammatory cytokine levels, altered bacterial microbiota, and regulated lymphocyte proportions. FMT is effective in a mouse model of NEC through the modulation of oxidative stress and reduced colon inflammation.
DOI: 10.1016/j.freeradbiomed.2017.03.011
PubMed: 28323128
Affiliations:
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Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Li, Xiaowen" sort="Li, Xiaowen" uniqKey="Li X" first="Xiaowen" last="Li">Xiaowen Li</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Shang, Qingjuan" sort="Shang, Qingjuan" uniqKey="Shang Q" first="Qingjuan" last="Shang">Qingjuan Shang</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Gao, Zongwei" sort="Gao, Zongwei" uniqKey="Gao Z" first="Zongwei" last="Gao">Zongwei Gao</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Hao, Fabao" sort="Hao, Fabao" uniqKey="Hao F" first="Fabao" last="Hao">Fabao Hao</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Hongjie" sort="Guo, Hongjie" uniqKey="Guo H" first="Hongjie" last="Guo">Hongjie Guo</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China. Electronic address: guochunbao@foxmail.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Disease Progression (MeSH)</term><term>Enterocolitis, Necrotizing (immunology)</term><term>Enterocolitis, Necrotizing (therapy)</term><term>Fecal Microbiota Transplantation (MeSH)</term><term>Gastrointestinal Microbiome (immunology)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Humans (MeSH)</term><term>Inflammation (immunology)</term><term>Intestinal Mucosa (immunology)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Models, Animal (MeSH)</term><term>Nitric Oxide Synthase Type III (metabolism)</term><term>Oxidative Stress (MeSH)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Toll-Like Receptor 4 (metabolism)</term><term>Toll-Like Receptor 9 (metabolism)</term><term>Transcytosis (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Entérocolite nécrosante (immunologie)</term><term>Entérocolite nécrosante (thérapie)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Humains (MeSH)</term><term>Inflammation (immunologie)</term><term>Microbiome gastro-intestinal (immunologie)</term><term>Modèles animaux (MeSH)</term><term>Muqueuse intestinale (immunologie)</term><term>Nitric oxide synthase type III (métabolisme)</term><term>Récepteur de type Toll-4 (métabolisme)</term><term>Récepteur-9 de type Toll-like (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term><term>Stress oxydatif (MeSH)</term><term>Transcytose (MeSH)</term><term>Transduction du signal (MeSH)</term><term>Transplantation de microbiote fécal (MeSH)</term><term>Évolution de la maladie (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Entérocolite nécrosante</term><term>Inflammation</term><term>Microbiome gastro-intestinal</term><term>Muqueuse intestinale</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Enterocolitis, Necrotizing</term><term>Gastrointestinal Microbiome</term><term>Inflammation</term><term>Intestinal Mucosa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term><term>Nitric Oxide Synthase Type III</term><term>Reactive Oxygen Species</term><term>Toll-Like Receptor 4</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term><term>Glutarédoxines</term><term>Nitric oxide synthase type III</term><term>Récepteur de type Toll-4</term><term>Récepteur-9 de type Toll-like</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Enterocolitis, Necrotizing</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Entérocolite nécrosante</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Progression</term><term>Fecal Microbiota Transplantation</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Models, Animal</term><term>Oxidative Stress</term><term>Signal Transduction</term><term>Transcytosis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Stress oxydatif</term><term>Transcytose</term><term>Transduction du signal</term><term>Transplantation de microbiote fécal</term><term>Évolution de la maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fecal microbiota transplantation (FMT) has been used successfully to treat a variety of gastroenterological diseases. The alterations of microbiota in mouse models of necrotizing enterocolitis (NEC) as well as in patients suggested the possibility of treating NEC with FMT. Here we show that FMT caused an improvement in the histopathology and symptoms of NEC in WT mice, but not Grx1-/- mice. FMT eliminated O<sub>2</sub><sup>•</sup>- production and promoted NO production in experimental NEC mice though the modulation of S-glutathionylation of eNOS (eNOS-SSG). FMT decreased the extent of TLR4-mediated proinflammatory signaling though TLR9 in the intestinal mucosa tissue. FMT also suppressed intestinal apoptosis and bacterial translocation across the intestinal barrier, which was accompanied by decreased inflammatory cytokine levels, altered bacterial microbiota, and regulated lymphocyte proportions. FMT is effective in a mouse model of NEC through the modulation of oxidative stress and reduced colon inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28323128</PMID><DateCompleted><Year>2018</Year><Month>03</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>04</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>108</Volume><PubDate><Year>2017</Year><Month>07</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Fecal microbiota transplantation (FMT) could reverse the severity of experimental necrotizing enterocolitis (NEC) via oxidative stress modulation.</ArticleTitle><Pagination><MedlinePgn>32-43</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(17)30135-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2017.03.011</ELocationID><Abstract><AbstractText>Fecal microbiota transplantation (FMT) has been used successfully to treat a variety of gastroenterological diseases. The alterations of microbiota in mouse models of necrotizing enterocolitis (NEC) as well as in patients suggested the possibility of treating NEC with FMT. Here we show that FMT caused an improvement in the histopathology and symptoms of NEC in WT mice, but not Grx1-/- mice. FMT eliminated O<sub>2</sub><sup>•</sup>- production and promoted NO production in experimental NEC mice though the modulation of S-glutathionylation of eNOS (eNOS-SSG). FMT decreased the extent of TLR4-mediated proinflammatory signaling though TLR9 in the intestinal mucosa tissue. FMT also suppressed intestinal apoptosis and bacterial translocation across the intestinal barrier, which was accompanied by decreased inflammatory cytokine levels, altered bacterial microbiota, and regulated lymphocyte proportions. FMT is effective in a mouse model of NEC through the modulation of oxidative stress and reduced colon inflammation.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xiaomei</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xiaowen</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shang</LastName><ForeName>Qingjuan</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Zongwei</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Department of Pathology, Linyi People's Hospital, Linyi, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hao</LastName><ForeName>Fabao</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Hongjie</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Chunbao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China. Electronic address: guochunbao@foxmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>03</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493487">Tlr4 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495370">Tlr9 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051217">Toll-Like Receptor 9</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052250">Nitric Oxide Synthase Type III</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020345" MajorTopicYN="N">Enterocolitis, Necrotizing</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069467" MajorTopicYN="Y">Fecal Microbiota Transplantation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="N">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007413" MajorTopicYN="N">Intestinal Mucosa</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D023421" MajorTopicYN="N">Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052250" MajorTopicYN="N">Nitric Oxide Synthase Type III</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051197" MajorTopicYN="N">Toll-Like Receptor 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051217" MajorTopicYN="N">Toll-Like Receptor 9</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057900" MajorTopicYN="N">Transcytosis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">FMT</Keyword><Keyword MajorTopicYN="Y">NO</Keyword><Keyword MajorTopicYN="Y">S-glutathionylation</Keyword><Keyword MajorTopicYN="Y">TLR4</Keyword><Keyword MajorTopicYN="Y">eNOS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>03</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>03</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>3</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>3</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28323128</ArticleId><ArticleId IdType="pii">S0891-5849(17)30135-1</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2017.03.011</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, Xiaomei" sort="Li, Xiaomei" uniqKey="Li X" first="Xiaomei" last="Li">Xiaomei Li</name></noRegion><name sortKey="Gao, Zongwei" sort="Gao, Zongwei" uniqKey="Gao Z" first="Zongwei" last="Gao">Zongwei Gao</name><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><name sortKey="Guo, Hongjie" sort="Guo, Hongjie" uniqKey="Guo H" first="Hongjie" last="Guo">Hongjie Guo</name><name sortKey="Hao, Fabao" sort="Hao, Fabao" uniqKey="Hao F" first="Fabao" last="Hao">Fabao Hao</name><name sortKey="Li, Xiaowen" sort="Li, Xiaowen" uniqKey="Li X" first="Xiaowen" last="Li">Xiaowen Li</name><name sortKey="Shang, Qingjuan" sort="Shang, Qingjuan" uniqKey="Shang Q" first="Qingjuan" 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