Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis
The intracellular sensor NOD1 has important host-defense functions relating to a variety of pathogens. Here, we showed that this molecule also participates in the induction of a noninfectious pancreatitis via its response to commensal organisms. Pancreatitis induced by high-dose cerulein (a cholecys...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2012-08, Vol.37 (2), p.326-338 |
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| creator | Tsuji, Yoshihisa Watanabe, Tomohiro Kudo, Masatoshi Arai, Hidenori Strober, Warren Chiba, Tsutomu |
| description | The intracellular sensor NOD1 has important host-defense functions relating to a variety of pathogens. Here, we showed that this molecule also participates in the induction of a noninfectious pancreatitis via its response to commensal organisms. Pancreatitis induced by high-dose cerulein (a cholecystokinin receptor agonist) administration depends on NOD1 stimulation by gut microflora. To analyze this NOD1 activity, we induced pancreatitis by simultaneous administration of a low dose of cerulein (that does not itself induce pancreatitis) and FK156, an activator of NOD1 that mimics the effect of gut bacteria that have breached the mucosal barrier. The pancreatitis was dependent on acinar cell production of the chemokine MCP-1 and the intrapancreatic influx of CCR2+ inflammatory cells. Moreover, MCP-1 production involved activation of the transcription factors NF-κB and STAT3, each requiring complementary NOD1 and cerulein signaling. These studies indicate that gut commensals enable noninfectious pancreatic inflammation via NOD1 signaling in pancreatic acinar cells.
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► NOD1 activation enhances a cholecystokinin receptor agonist-induced pancreatitis ► The development of pancreatitis depends on the interaction between CCR2 and MCP-1 ► Activation of STAT3 and NF-κB is responsible for the development of pancreatitis ► Commensal organisms facilitate pancreatic inflammation via NOD1 signaling |
| doi_str_mv | 10.1016/j.immuni.2012.05.024 |
| format | Article |
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[Display omitted]
► NOD1 activation enhances a cholecystokinin receptor agonist-induced pancreatitis ► The development of pancreatitis depends on the interaction between CCR2 and MCP-1 ► Activation of STAT3 and NF-κB is responsible for the development of pancreatitis ► Commensal organisms facilitate pancreatic inflammation via NOD1 signaling</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2012.05.024</identifier><identifier>PMID: 22902233</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acetylmuramyl-Alanyl-Isoglutamine - adverse effects ; Acinar cells ; Acinar Cells - immunology ; Animals ; Antibiotics ; Bacteria - immunology ; Ceruletide - adverse effects ; Chemokine CCL2 - biosynthesis ; Chemokine CCL2 - immunology ; Chemokines ; Cholecystokinin receptors ; Commensals ; Diaminopimelic Acid - adverse effects ; Diaminopimelic Acid - analogs & derivatives ; Digestive tract ; Enzymes ; Experiments ; Humans ; Immunity, Mucosal - immunology ; Inflammation ; Metabolic disorders ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microflora ; Monocyte chemoattractant protein 1 ; Mortality ; Mucosa ; Mucous Membrane - immunology ; Mucous Membrane - microbiology ; NF- Kappa B protein ; NF-kappa B - metabolism ; Nod1 protein ; Nod1 Signaling Adaptor Protein - immunology ; Nod1 Signaling Adaptor Protein - metabolism ; Organisms ; Pancreas ; Pancreatitis ; Pancreatitis - chemically induced ; Pancreatitis - immunology ; Pathogens ; Receptors, CCR2 - biosynthesis ; Receptors, CCR2 - immunology ; Rodents ; Signal Transduction - immunology ; Stat3 protein ; STAT3 Transcription Factor - metabolism ; Transcription factors</subject><ispartof>Immunity (Cambridge, Mass.), 2012-08, Vol.37 (2), p.326-338</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Aug 24, 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-a7de43e0695f782be329eda7c7ee1fbe5b7741519e65dc5c050ef2065fa6197b3</citedby><cites>FETCH-LOGICAL-c590t-a7de43e0695f782be329eda7c7ee1fbe5b7741519e65dc5c050ef2065fa6197b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.immuni.2012.05.024$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22902233$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsuji, Yoshihisa</creatorcontrib><creatorcontrib>Watanabe, Tomohiro</creatorcontrib><creatorcontrib>Kudo, Masatoshi</creatorcontrib><creatorcontrib>Arai, Hidenori</creatorcontrib><creatorcontrib>Strober, Warren</creatorcontrib><creatorcontrib>Chiba, Tsutomu</creatorcontrib><title>Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>The intracellular sensor NOD1 has important host-defense functions relating to a variety of pathogens. Here, we showed that this molecule also participates in the induction of a noninfectious pancreatitis via its response to commensal organisms. Pancreatitis induced by high-dose cerulein (a cholecystokinin receptor agonist) administration depends on NOD1 stimulation by gut microflora. To analyze this NOD1 activity, we induced pancreatitis by simultaneous administration of a low dose of cerulein (that does not itself induce pancreatitis) and FK156, an activator of NOD1 that mimics the effect of gut bacteria that have breached the mucosal barrier. The pancreatitis was dependent on acinar cell production of the chemokine MCP-1 and the intrapancreatic influx of CCR2+ inflammatory cells. Moreover, MCP-1 production involved activation of the transcription factors NF-κB and STAT3, each requiring complementary NOD1 and cerulein signaling. These studies indicate that gut commensals enable noninfectious pancreatic inflammation via NOD1 signaling in pancreatic acinar cells.
[Display omitted]
► NOD1 activation enhances a cholecystokinin receptor agonist-induced pancreatitis ► The development of pancreatitis depends on the interaction between CCR2 and MCP-1 ► Activation of STAT3 and NF-κB is responsible for the development of pancreatitis ► Commensal organisms facilitate pancreatic inflammation via NOD1 signaling</description><subject>Acetylmuramyl-Alanyl-Isoglutamine - adverse effects</subject><subject>Acinar cells</subject><subject>Acinar Cells - immunology</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Bacteria - immunology</subject><subject>Ceruletide - adverse effects</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CCL2 - immunology</subject><subject>Chemokines</subject><subject>Cholecystokinin receptors</subject><subject>Commensals</subject><subject>Diaminopimelic Acid - adverse effects</subject><subject>Diaminopimelic Acid - analogs & derivatives</subject><subject>Digestive tract</subject><subject>Enzymes</subject><subject>Experiments</subject><subject>Humans</subject><subject>Immunity, Mucosal - immunology</subject><subject>Inflammation</subject><subject>Metabolic disorders</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microflora</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Mortality</subject><subject>Mucosa</subject><subject>Mucous Membrane - immunology</subject><subject>Mucous Membrane - microbiology</subject><subject>NF- Kappa B protein</subject><subject>NF-kappa B - metabolism</subject><subject>Nod1 protein</subject><subject>Nod1 Signaling Adaptor Protein - immunology</subject><subject>Nod1 Signaling Adaptor Protein - metabolism</subject><subject>Organisms</subject><subject>Pancreas</subject><subject>Pancreatitis</subject><subject>Pancreatitis - chemically induced</subject><subject>Pancreatitis - immunology</subject><subject>Pathogens</subject><subject>Receptors, CCR2 - biosynthesis</subject><subject>Receptors, CCR2 - immunology</subject><subject>Rodents</subject><subject>Signal Transduction - immunology</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Transcription factors</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhSMEoqXwBghZYsMmwdeJ43iDhKYFKhUGCVhbjnMz9SixB9up6NvjaEr5WbCyLZ97fI6_ongOtAIK7et9Zed5cbZiFFhFeUVZ86A4BSpF2UBHH6570ZSihfqkeBLjnlJouKSPixPGJGWsrk-L_gu6aN2O-JFs_Dznk57INuy0s3GOpL8l6RrJpUtBG5ymZdKBrDM-kE_bcyAfcbA6YSQXPw4YbDZI2eCzdiagTjbZ-LR4NOop4rO79az49u7i6-ZDebV9f7l5e1WaHCqVWgzY1EhbyUfRsR5rJnHQwghEGHvkvRANcJDY8sFwQznFkdGWj7oFKfr6rHhz9D0s_YyDwTXzpA45lA63ymur_r5x9lrt_I2qOau7jmeDV3cGwX9fMCY127iW1g79EhUA1AwEFZClL_-R7v0SXK6noGVSyoZ3NKuao8oEH2PA8T4MULVCVHt1hKhWiIpylSHmsRd_Frkf-kXtd1PM33ljMahoLDqTUQQ0SQ3e_v-FnwH9sR4</recordid><startdate>20120824</startdate><enddate>20120824</enddate><creator>Tsuji, Yoshihisa</creator><creator>Watanabe, Tomohiro</creator><creator>Kudo, Masatoshi</creator><creator>Arai, Hidenori</creator><creator>Strober, Warren</creator><creator>Chiba, Tsutomu</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20120824</creationdate><title>Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis</title><author>Tsuji, Yoshihisa ; Watanabe, Tomohiro ; Kudo, Masatoshi ; Arai, Hidenori ; Strober, Warren ; Chiba, Tsutomu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-a7de43e0695f782be329eda7c7ee1fbe5b7741519e65dc5c050ef2065fa6197b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetylmuramyl-Alanyl-Isoglutamine - adverse effects</topic><topic>Acinar cells</topic><topic>Acinar Cells - immunology</topic><topic>Animals</topic><topic>Antibiotics</topic><topic>Bacteria - immunology</topic><topic>Ceruletide - adverse effects</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Chemokine CCL2 - immunology</topic><topic>Chemokines</topic><topic>Cholecystokinin receptors</topic><topic>Commensals</topic><topic>Diaminopimelic Acid - adverse effects</topic><topic>Diaminopimelic Acid - analogs & derivatives</topic><topic>Digestive tract</topic><topic>Enzymes</topic><topic>Experiments</topic><topic>Humans</topic><topic>Immunity, Mucosal - immunology</topic><topic>Inflammation</topic><topic>Metabolic disorders</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Microflora</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Mortality</topic><topic>Mucosa</topic><topic>Mucous Membrane - immunology</topic><topic>Mucous Membrane - microbiology</topic><topic>NF- Kappa B protein</topic><topic>NF-kappa B - metabolism</topic><topic>Nod1 protein</topic><topic>Nod1 Signaling Adaptor Protein - immunology</topic><topic>Nod1 Signaling Adaptor Protein - metabolism</topic><topic>Organisms</topic><topic>Pancreas</topic><topic>Pancreatitis</topic><topic>Pancreatitis - chemically induced</topic><topic>Pancreatitis - immunology</topic><topic>Pathogens</topic><topic>Receptors, CCR2 - biosynthesis</topic><topic>Receptors, CCR2 - immunology</topic><topic>Rodents</topic><topic>Signal Transduction - immunology</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsuji, Yoshihisa</creatorcontrib><creatorcontrib>Watanabe, Tomohiro</creatorcontrib><creatorcontrib>Kudo, Masatoshi</creatorcontrib><creatorcontrib>Arai, Hidenori</creatorcontrib><creatorcontrib>Strober, Warren</creatorcontrib><creatorcontrib>Chiba, Tsutomu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsuji, Yoshihisa</au><au>Watanabe, Tomohiro</au><au>Kudo, Masatoshi</au><au>Arai, Hidenori</au><au>Strober, Warren</au><au>Chiba, Tsutomu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>2012-08-24</date><risdate>2012</risdate><volume>37</volume><issue>2</issue><spage>326</spage><epage>338</epage><pages>326-338</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>The intracellular sensor NOD1 has important host-defense functions relating to a variety of pathogens. Here, we showed that this molecule also participates in the induction of a noninfectious pancreatitis via its response to commensal organisms. Pancreatitis induced by high-dose cerulein (a cholecystokinin receptor agonist) administration depends on NOD1 stimulation by gut microflora. To analyze this NOD1 activity, we induced pancreatitis by simultaneous administration of a low dose of cerulein (that does not itself induce pancreatitis) and FK156, an activator of NOD1 that mimics the effect of gut bacteria that have breached the mucosal barrier. The pancreatitis was dependent on acinar cell production of the chemokine MCP-1 and the intrapancreatic influx of CCR2+ inflammatory cells. Moreover, MCP-1 production involved activation of the transcription factors NF-κB and STAT3, each requiring complementary NOD1 and cerulein signaling. These studies indicate that gut commensals enable noninfectious pancreatic inflammation via NOD1 signaling in pancreatic acinar cells.
[Display omitted]
► NOD1 activation enhances a cholecystokinin receptor agonist-induced pancreatitis ► The development of pancreatitis depends on the interaction between CCR2 and MCP-1 ► Activation of STAT3 and NF-κB is responsible for the development of pancreatitis ► Commensal organisms facilitate pancreatic inflammation via NOD1 signaling</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22902233</pmid><doi>10.1016/j.immuni.2012.05.024</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylmuramyl-Alanyl-Isoglutamine - adverse effects Acinar cells Acinar Cells - immunology Animals Antibiotics Bacteria - immunology Ceruletide - adverse effects Chemokine CCL2 - biosynthesis Chemokine CCL2 - immunology Chemokines Cholecystokinin receptors Commensals Diaminopimelic Acid - adverse effects Diaminopimelic Acid - analogs & derivatives Digestive tract Enzymes Experiments Humans Immunity, Mucosal - immunology Inflammation Metabolic disorders Mice Mice, Inbred C57BL Mice, Transgenic Microflora Monocyte chemoattractant protein 1 Mortality Mucosa Mucous Membrane - immunology Mucous Membrane - microbiology NF- Kappa B protein NF-kappa B - metabolism Nod1 protein Nod1 Signaling Adaptor Protein - immunology Nod1 Signaling Adaptor Protein - metabolism Organisms Pancreas Pancreatitis Pancreatitis - chemically induced Pancreatitis - immunology Pathogens Receptors, CCR2 - biosynthesis Receptors, CCR2 - immunology Rodents Signal Transduction - immunology Stat3 protein STAT3 Transcription Factor - metabolism Transcription factors |
| title | Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis |
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