Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis
Although genetic polymorphisms in NOD2 (nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn’s disease (CD), little is known regarding the role of wild-type (WT) NOD2 in the gut. To date, most murine studies addressing the role of WT Nod2 have b...
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| Veröffentlicht in: | Mucosal immunology 2017-07, Vol.10 (4), p.971-982 |
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| creator | Corridoni, D Rodriguez-Palacios, A Di Stefano, G Di Martino, L Antonopoulos, D A Chang, E B Arseneau, K O Pizarro, T T Cominelli, F |
| description | Although genetic polymorphisms in
NOD2
(nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn’s disease (CD), little is known regarding the role of wild-type (WT)
NOD2
in the gut. To date, most murine studies addressing the role of WT
Nod2
have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of
Nod2
deletion in a murine model of spontaneous ileitis, i.e., the SAMP1Yit/Fc (SAMP) strain, which closely resembles CD. Remarkably,
Nod2
deletion improved both chronic cobblestone ileitis (by 50% assessed, as the % of abnormal mucosa at 24 wks of age), as well as acute dextran sodium sulfate (DSS) colitis. Mechanistically, Th2 cytokine production and Th2-transcription factor activation (i.e., STAT6 phosphorylation) were reduced. Microbiologically, the effects of
Nod2
deletion appeared independent of fecal microbiota composition and function, assessed by 16S rRNA and metatranscriptomics. Our findings indicate that pharmacological blockade of NOD2 signaling in humans could improve health in Th2-driven chronic intestinal inflammation. |
| doi_str_mv | 10.1038/mi.2016.98 |
| format | Article |
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NOD2
(nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn’s disease (CD), little is known regarding the role of wild-type (WT)
NOD2
in the gut. To date, most murine studies addressing the role of WT
Nod2
have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of
Nod2
deletion in a murine model of spontaneous ileitis, i.e., the SAMP1Yit/Fc (SAMP) strain, which closely resembles CD. Remarkably,
Nod2
deletion improved both chronic cobblestone ileitis (by 50% assessed, as the % of abnormal mucosa at 24 wks of age), as well as acute dextran sodium sulfate (DSS) colitis. Mechanistically, Th2 cytokine production and Th2-transcription factor activation (i.e., STAT6 phosphorylation) were reduced. Microbiologically, the effects of
Nod2
deletion appeared independent of fecal microbiota composition and function, assessed by 16S rRNA and metatranscriptomics. Our findings indicate that pharmacological blockade of NOD2 signaling in humans could improve health in Th2-driven chronic intestinal inflammation.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/mi.2016.98</identifier><identifier>PMID: 27848951</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/347 ; 631/45/612/1234 ; 692/4020/1503/2745 ; 692/699/249/2510/257/1402 ; Allergology ; Animal models ; Animals ; Antibodies ; Biomedical and Life Sciences ; Biomedicine ; Colitis ; Colitis - chemically induced ; Colitis - genetics ; Colitis - microbiology ; Colon ; Crohn Disease - genetics ; Crohn Disease - immunology ; Crohn Disease - microbiology ; Crohn's disease ; Cytokines - metabolism ; Dextran ; Dextran Sulfate ; Disease Models, Animal ; Disease Susceptibility ; Dysbacteriosis ; Dysbiosis ; Fecal microflora ; Feces - microbiology ; Gastroenterology ; Humans ; Ileitis ; Ileitis - genetics ; Ileitis - immunology ; Ileitis - microbiology ; Immunology ; Inflammatory bowel disease ; Intestinal Mucosa - pathology ; Intestine ; Lymphocytes T ; Mice ; Mice, Knockout ; Mice, Mutant Strains ; Microbiota ; Microbiota - genetics ; Mucosa ; NOD2 protein ; Nod2 Signaling Adaptor Protein - genetics ; Nod2 Signaling Adaptor Protein - metabolism ; Oligomerization ; Phosphorylation ; Receptors, Pattern Recognition - genetics ; Receptors, Pattern Recognition - metabolism ; RNA, Ribosomal, 16S - analysis ; Rodents ; rRNA 16S ; Sodium sulfate ; Stat6 protein ; STAT6 Transcription Factor - metabolism ; Transcription activation</subject><ispartof>Mucosal immunology, 2017-07, Vol.10 (4), p.971-982</ispartof><rights>Society for Mucosal Immunology 2017</rights><rights>Copyright Nature Publishing Group Jul 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-915532afacaee618aec10a6d0d3531b705e6a2e160482f398095e024bca77de03</citedby><cites>FETCH-LOGICAL-c535t-915532afacaee618aec10a6d0d3531b705e6a2e160482f398095e024bca77de03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1910313648?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,64384,64388,72240</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27848951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/1427533$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Corridoni, D</creatorcontrib><creatorcontrib>Rodriguez-Palacios, A</creatorcontrib><creatorcontrib>Di Stefano, G</creatorcontrib><creatorcontrib>Di Martino, L</creatorcontrib><creatorcontrib>Antonopoulos, D A</creatorcontrib><creatorcontrib>Chang, E B</creatorcontrib><creatorcontrib>Arseneau, K O</creatorcontrib><creatorcontrib>Pizarro, T T</creatorcontrib><creatorcontrib>Cominelli, F</creatorcontrib><creatorcontrib>Argonne National Lab. (ANL), Argonne, IL (United States)</creatorcontrib><title>Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><addtitle>Mucosal Immunol</addtitle><description>Although genetic polymorphisms in
NOD2
(nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn’s disease (CD), little is known regarding the role of wild-type (WT)
NOD2
in the gut. To date, most murine studies addressing the role of WT
Nod2
have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of
Nod2
deletion in a murine model of spontaneous ileitis, i.e., the SAMP1Yit/Fc (SAMP) strain, which closely resembles CD. Remarkably,
Nod2
deletion improved both chronic cobblestone ileitis (by 50% assessed, as the % of abnormal mucosa at 24 wks of age), as well as acute dextran sodium sulfate (DSS) colitis. Mechanistically, Th2 cytokine production and Th2-transcription factor activation (i.e., STAT6 phosphorylation) were reduced. Microbiologically, the effects of
Nod2
deletion appeared independent of fecal microbiota composition and function, assessed by 16S rRNA and metatranscriptomics. Our findings indicate that pharmacological blockade of NOD2 signaling in humans could improve health in Th2-driven chronic intestinal inflammation.</description><subject>631/250/347</subject><subject>631/45/612/1234</subject><subject>692/4020/1503/2745</subject><subject>692/699/249/2510/257/1402</subject><subject>Allergology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Colitis</subject><subject>Colitis - chemically induced</subject><subject>Colitis - genetics</subject><subject>Colitis - microbiology</subject><subject>Colon</subject><subject>Crohn Disease - genetics</subject><subject>Crohn Disease - immunology</subject><subject>Crohn Disease - microbiology</subject><subject>Crohn's disease</subject><subject>Cytokines - metabolism</subject><subject>Dextran</subject><subject>Dextran Sulfate</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis</subject><subject>Fecal microflora</subject><subject>Feces - microbiology</subject><subject>Gastroenterology</subject><subject>Humans</subject><subject>Ileitis</subject><subject>Ileitis - genetics</subject><subject>Ileitis - immunology</subject><subject>Ileitis - microbiology</subject><subject>Immunology</subject><subject>Inflammatory bowel disease</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Mutant Strains</subject><subject>Microbiota</subject><subject>Microbiota - genetics</subject><subject>Mucosa</subject><subject>NOD2 protein</subject><subject>Nod2 Signaling Adaptor Protein - genetics</subject><subject>Nod2 Signaling Adaptor Protein - metabolism</subject><subject>Oligomerization</subject><subject>Phosphorylation</subject><subject>Receptors, Pattern Recognition - genetics</subject><subject>Receptors, Pattern Recognition - metabolism</subject><subject>RNA, Ribosomal, 16S - analysis</subject><subject>Rodents</subject><subject>rRNA 16S</subject><subject>Sodium sulfate</subject><subject>Stat6 protein</subject><subject>STAT6 Transcription Factor - metabolism</subject><subject>Transcription activation</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkc1u1TAQhSMEoj-w4QGQBbtWufgnTuJNJXSBglTRDawtx5n0uiT2xeNU6q6vwevxJDi9pWrVjcfSfDrnjE5RvGF0xahoP0xuxSmrV6p9VuwzJWQpKlk_v_2LknKm9ooDxEtKa0qleFns8aatWiXZfnFzCh6Ss6SHMc_gSRhI2gDpjE0QnRkJgscQyffzT5y4aRvDFSCZ5ug8kHUMG__35g-S3iEYhHJ0v4C4EVxySJzvYQv58WnRHWZvF48s2l9j5wI6fFW8GMyI8PpuHhY_v3z-sf5anp2fflt_PCutFDKVikkpuBmMNQA1aw1YRk3d015IwbqGSqgNB1bTquWDUC1VEiivOmuapgcqDouTne527ibobY4Uzai30U0mXutgnH688W6jL8KVlpUQirMs8G4nEDA5jdYlsBsbvAebNKt4I4XI0Ps7lxh-z4BJX4Y55oNRM5XLYqKu2kwd7SgbA2KE4T4Go3qpVE9OL5VqtcBvHwa_R_93mIHjHYB55S8gPvB8KvcPEbet3w</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Corridoni, D</creator><creator>Rodriguez-Palacios, A</creator><creator>Di Stefano, G</creator><creator>Di Martino, L</creator><creator>Antonopoulos, D A</creator><creator>Chang, E B</creator><creator>Arseneau, K O</creator><creator>Pizarro, T T</creator><creator>Cominelli, F</creator><general>Nature Publishing Group US</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>20170701</creationdate><title>Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis</title><author>Corridoni, D ; Rodriguez-Palacios, A ; Di Stefano, G ; Di Martino, L ; Antonopoulos, D A ; Chang, E B ; Arseneau, K O ; Pizarro, T T ; Cominelli, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-915532afacaee618aec10a6d0d3531b705e6a2e160482f398095e024bca77de03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>631/250/347</topic><topic>631/45/612/1234</topic><topic>692/4020/1503/2745</topic><topic>692/699/249/2510/257/1402</topic><topic>Allergology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Colitis</topic><topic>Colitis - chemically induced</topic><topic>Colitis - genetics</topic><topic>Colitis - microbiology</topic><topic>Colon</topic><topic>Crohn Disease - genetics</topic><topic>Crohn Disease - immunology</topic><topic>Crohn Disease - microbiology</topic><topic>Crohn's disease</topic><topic>Cytokines - metabolism</topic><topic>Dextran</topic><topic>Dextran Sulfate</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility</topic><topic>Dysbacteriosis</topic><topic>Dysbiosis</topic><topic>Fecal microflora</topic><topic>Feces - microbiology</topic><topic>Gastroenterology</topic><topic>Humans</topic><topic>Ileitis</topic><topic>Ileitis - genetics</topic><topic>Ileitis - immunology</topic><topic>Ileitis - microbiology</topic><topic>Immunology</topic><topic>Inflammatory bowel disease</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Mutant Strains</topic><topic>Microbiota</topic><topic>Microbiota - genetics</topic><topic>Mucosa</topic><topic>NOD2 protein</topic><topic>Nod2 Signaling Adaptor Protein - genetics</topic><topic>Nod2 Signaling Adaptor Protein - metabolism</topic><topic>Oligomerization</topic><topic>Phosphorylation</topic><topic>Receptors, Pattern Recognition - genetics</topic><topic>Receptors, Pattern Recognition - metabolism</topic><topic>RNA, Ribosomal, 16S - analysis</topic><topic>Rodents</topic><topic>rRNA 16S</topic><topic>Sodium sulfate</topic><topic>Stat6 protein</topic><topic>STAT6 Transcription Factor - metabolism</topic><topic>Transcription activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Corridoni, D</creatorcontrib><creatorcontrib>Rodriguez-Palacios, A</creatorcontrib><creatorcontrib>Di Stefano, G</creatorcontrib><creatorcontrib>Di Martino, L</creatorcontrib><creatorcontrib>Antonopoulos, D A</creatorcontrib><creatorcontrib>Chang, E B</creatorcontrib><creatorcontrib>Arseneau, K O</creatorcontrib><creatorcontrib>Pizarro, T T</creatorcontrib><creatorcontrib>Cominelli, F</creatorcontrib><creatorcontrib>Argonne National Lab. 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(ANL), Argonne, IL (United States)</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><addtitle>Mucosal Immunol</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>10</volume><issue>4</issue><spage>971</spage><epage>982</epage><pages>971-982</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>Although genetic polymorphisms in
NOD2
(nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn’s disease (CD), little is known regarding the role of wild-type (WT)
NOD2
in the gut. To date, most murine studies addressing the role of WT
Nod2
have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of
Nod2
deletion in a murine model of spontaneous ileitis, i.e., the SAMP1Yit/Fc (SAMP) strain, which closely resembles CD. Remarkably,
Nod2
deletion improved both chronic cobblestone ileitis (by 50% assessed, as the % of abnormal mucosa at 24 wks of age), as well as acute dextran sodium sulfate (DSS) colitis. Mechanistically, Th2 cytokine production and Th2-transcription factor activation (i.e., STAT6 phosphorylation) were reduced. Microbiologically, the effects of
Nod2
deletion appeared independent of fecal microbiota composition and function, assessed by 16S rRNA and metatranscriptomics. Our findings indicate that pharmacological blockade of NOD2 signaling in humans could improve health in Th2-driven chronic intestinal inflammation.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>27848951</pmid><doi>10.1038/mi.2016.98</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Mucosal immunology, 2017-07, Vol.10 (4), p.971-982 |
| issn | 1933-0219 1935-3456 |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5433921 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
| subjects | 631/250/347 631/45/612/1234 692/4020/1503/2745 692/699/249/2510/257/1402 Allergology Animal models Animals Antibodies Biomedical and Life Sciences Biomedicine Colitis Colitis - chemically induced Colitis - genetics Colitis - microbiology Colon Crohn Disease - genetics Crohn Disease - immunology Crohn Disease - microbiology Crohn's disease Cytokines - metabolism Dextran Dextran Sulfate Disease Models, Animal Disease Susceptibility Dysbacteriosis Dysbiosis Fecal microflora Feces - microbiology Gastroenterology Humans Ileitis Ileitis - genetics Ileitis - immunology Ileitis - microbiology Immunology Inflammatory bowel disease Intestinal Mucosa - pathology Intestine Lymphocytes T Mice Mice, Knockout Mice, Mutant Strains Microbiota Microbiota - genetics Mucosa NOD2 protein Nod2 Signaling Adaptor Protein - genetics Nod2 Signaling Adaptor Protein - metabolism Oligomerization Phosphorylation Receptors, Pattern Recognition - genetics Receptors, Pattern Recognition - metabolism RNA, Ribosomal, 16S - analysis Rodents rRNA 16S Sodium sulfate Stat6 protein STAT6 Transcription Factor - metabolism Transcription activation |
| title | Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis |
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