Interleukin‐22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice
Summary Our previous work has shown the significant up‐regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STA...
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| Veröffentlicht in: | Immunology 2015-04, Vol.144 (4), p.587-597 |
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| creator | Sadighi Akha, Amir A. McDermott, Andrew J. Theriot, Casey M. Carlson, Paul E. Frank, Charles R. McDonald, Roderick A. Falkowski, Nicole R. Bergin, Ingrid L. Young, Vincent B. Huffnagle, Gary B. |
| description | Summary
Our previous work has shown the significant up‐regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes interleukin‐22 (IL‐22) and CD160‐mediated components. The current study sought to determine the potential role(s) of IL‐22 and/or CD160 in the mucosal response to C. difficile infection. Clostridium difficile‐infected mice treated with anti‐IL‐22, anti‐CD160 or a combination of the two showed significantly reduced STAT3 phosphorylation in comparison to C. difficile‐infected mice that had not received either antibody. In addition, C. difficile‐infected mice treated with anti‐IL‐22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile‐infected mice. The affected genes included pro‐inflammatory chemokines and cytokines, and anti‐microbial peptides. Furthermore, histopathological and flow cytometric assessments both showed a significantly reduced influx of neutrophils in C. difficile‐infected mice treated with anti‐IL‐22/CD160. These data demonstrate that IL‐22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL‐22 and CD160 in mediating both the pro‐inflammatory and pro‐survival aspects of the host mucosal response in this infection. |
| doi_str_mv | 10.1111/imm.12414 |
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Our previous work has shown the significant up‐regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes interleukin‐22 (IL‐22) and CD160‐mediated components. The current study sought to determine the potential role(s) of IL‐22 and/or CD160 in the mucosal response to C. difficile infection. Clostridium difficile‐infected mice treated with anti‐IL‐22, anti‐CD160 or a combination of the two showed significantly reduced STAT3 phosphorylation in comparison to C. difficile‐infected mice that had not received either antibody. In addition, C. difficile‐infected mice treated with anti‐IL‐22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile‐infected mice. The affected genes included pro‐inflammatory chemokines and cytokines, and anti‐microbial peptides. Furthermore, histopathological and flow cytometric assessments both showed a significantly reduced influx of neutrophils in C. difficile‐infected mice treated with anti‐IL‐22/CD160. These data demonstrate that IL‐22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL‐22 and CD160 in mediating both the pro‐inflammatory and pro‐survival aspects of the host mucosal response in this infection.</description><identifier>ISSN: 0019-2805</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1111/imm.12414</identifier><identifier>PMID: 25327211</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animals ; Anti-Bacterial Agents ; Antibodies - pharmacology ; Antigens, CD - genetics ; Antigens, CD - immunology ; Antigens, CD - metabolism ; CD160 ; Clostridioides difficile - immunology ; Clostridioides difficile - pathogenicity ; Clostridium difficile ; Disease Models, Animal ; Enterocolitis, Pseudomembranous - genetics ; Enterocolitis, Pseudomembranous - immunology ; Enterocolitis, Pseudomembranous - metabolism ; Enterocolitis, Pseudomembranous - microbiology ; Enterocolitis, Pseudomembranous - prevention & control ; Gene Expression Regulation ; GPI-Linked Proteins - antagonists & inhibitors ; GPI-Linked Proteins - genetics ; GPI-Linked Proteins - immunology ; GPI-Linked Proteins - metabolism ; Immunity, Mucosal - drug effects ; Interleukin-22 ; Interleukins - antagonists & inhibitors ; Interleukins - genetics ; Interleukins - immunology ; Interleukins - metabolism ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - immunology ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - microbiology ; Male ; Mice, Inbred C57BL ; Neutrophil Infiltration ; Original ; Phosphorylation ; pSTAT3 ; Receptors, Immunologic - antagonists & inhibitors ; Receptors, Immunologic - genetics ; Receptors, Immunologic - immunology ; Receptors, Immunologic - metabolism ; RegIIIγ ; Signal Transduction ; STAT3 Transcription Factor - immunology ; STAT3 Transcription Factor - metabolism ; Time Factors</subject><ispartof>Immunology, 2015-04, Vol.144 (4), p.587-597</ispartof><rights>2014 John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons Ltd.</rights><rights>Copyright © 2015 John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons Ltd 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4368165/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4368165/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25327211$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sadighi Akha, Amir A.</creatorcontrib><creatorcontrib>McDermott, Andrew J.</creatorcontrib><creatorcontrib>Theriot, Casey M.</creatorcontrib><creatorcontrib>Carlson, Paul E.</creatorcontrib><creatorcontrib>Frank, Charles R.</creatorcontrib><creatorcontrib>McDonald, Roderick A.</creatorcontrib><creatorcontrib>Falkowski, Nicole R.</creatorcontrib><creatorcontrib>Bergin, Ingrid L.</creatorcontrib><creatorcontrib>Young, Vincent B.</creatorcontrib><creatorcontrib>Huffnagle, Gary B.</creatorcontrib><title>Interleukin‐22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice</title><title>Immunology</title><addtitle>Immunology</addtitle><description>Summary
Our previous work has shown the significant up‐regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes interleukin‐22 (IL‐22) and CD160‐mediated components. The current study sought to determine the potential role(s) of IL‐22 and/or CD160 in the mucosal response to C. difficile infection. Clostridium difficile‐infected mice treated with anti‐IL‐22, anti‐CD160 or a combination of the two showed significantly reduced STAT3 phosphorylation in comparison to C. difficile‐infected mice that had not received either antibody. In addition, C. difficile‐infected mice treated with anti‐IL‐22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile‐infected mice. The affected genes included pro‐inflammatory chemokines and cytokines, and anti‐microbial peptides. Furthermore, histopathological and flow cytometric assessments both showed a significantly reduced influx of neutrophils in C. difficile‐infected mice treated with anti‐IL‐22/CD160. These data demonstrate that IL‐22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL‐22 and CD160 in mediating both the pro‐inflammatory and pro‐survival aspects of the host mucosal response in this infection.</description><subject>Animals</subject><subject>Anti-Bacterial Agents</subject><subject>Antibodies - pharmacology</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - immunology</subject><subject>Antigens, CD - metabolism</subject><subject>CD160</subject><subject>Clostridioides difficile - immunology</subject><subject>Clostridioides difficile - pathogenicity</subject><subject>Clostridium difficile</subject><subject>Disease Models, Animal</subject><subject>Enterocolitis, Pseudomembranous - genetics</subject><subject>Enterocolitis, Pseudomembranous - immunology</subject><subject>Enterocolitis, Pseudomembranous - metabolism</subject><subject>Enterocolitis, Pseudomembranous - microbiology</subject><subject>Enterocolitis, Pseudomembranous - prevention & control</subject><subject>Gene Expression Regulation</subject><subject>GPI-Linked Proteins - antagonists & inhibitors</subject><subject>GPI-Linked Proteins - genetics</subject><subject>GPI-Linked Proteins - immunology</subject><subject>GPI-Linked Proteins - metabolism</subject><subject>Immunity, Mucosal - drug effects</subject><subject>Interleukin-22</subject><subject>Interleukins - antagonists & inhibitors</subject><subject>Interleukins - genetics</subject><subject>Interleukins - immunology</subject><subject>Interleukins - metabolism</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - immunology</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Neutrophil Infiltration</subject><subject>Original</subject><subject>Phosphorylation</subject><subject>pSTAT3</subject><subject>Receptors, Immunologic - antagonists & inhibitors</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - immunology</subject><subject>Receptors, Immunologic - metabolism</subject><subject>RegIIIγ</subject><subject>Signal Transduction</subject><subject>STAT3 Transcription Factor - immunology</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Time Factors</subject><issn>0019-2805</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkcFu1DAQhi0EokvhwAsgS1y4bOuxYye5IKGlwEqtuPRuOc6E9eLYi51stTcegWfsk-BtSwX4Yo_-b37N-CfkNbAzKOfcjeMZ8AqqJ2QBQskll6p-ShaMQbvkDZMn5EXO21IKJuVzcsKl4DUHWJD9OkyYPM7fXbj9-YtzakJPVx9BMbrz5kBN37vJ7ZGm6DFTF-i0QbqJeaLjbGM2nibMuxgy0inSlS9Kcr2bR9q7YXDWeSxdA9rJxXDsH53Fl-TZYHzGVw_3Kbn-dHG9-rK8_Pp5vfpwudxWQlZlj0EawaHuhr6Xrewaa23LOquMENgI24qOtcoMdSsVMwJq7O3QKQDsGEdxSt7f2-7mbiwShikZr3fJjSYddDRO_6sEt9Hf4l5XQjWgZDF492CQ4o8Z86RHly16bwLGOWtQileCK9UW9O1_6DbOKZTtjhRUTSPhaPjm74keR_mTSAHO74Gb8nGHRx2YPkatS9T6Lmq9vrq6e4jfm_Cdbw</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>Sadighi Akha, Amir A.</creator><creator>McDermott, Andrew J.</creator><creator>Theriot, Casey M.</creator><creator>Carlson, Paul E.</creator><creator>Frank, Charles R.</creator><creator>McDonald, Roderick A.</creator><creator>Falkowski, Nicole R.</creator><creator>Bergin, Ingrid L.</creator><creator>Young, Vincent B.</creator><creator>Huffnagle, Gary B.</creator><general>Wiley Subscription Services, Inc</general><general>BlackWell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QR</scope><scope>7T5</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201504</creationdate><title>Interleukin‐22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice</title><author>Sadighi Akha, Amir A. ; McDermott, Andrew J. ; Theriot, Casey M. ; Carlson, Paul E. ; Frank, Charles R. ; McDonald, Roderick A. ; Falkowski, Nicole R. ; Bergin, Ingrid L. ; Young, Vincent B. ; Huffnagle, Gary B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j4354-25f5a3217bfdd595b8ccc90bc6a33e83c93b096af79560a317edcfb611eb02e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Anti-Bacterial Agents</topic><topic>Antibodies - pharmacology</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - immunology</topic><topic>Antigens, CD - metabolism</topic><topic>CD160</topic><topic>Clostridioides difficile - immunology</topic><topic>Clostridioides difficile - pathogenicity</topic><topic>Clostridium difficile</topic><topic>Disease Models, Animal</topic><topic>Enterocolitis, Pseudomembranous - genetics</topic><topic>Enterocolitis, Pseudomembranous - immunology</topic><topic>Enterocolitis, Pseudomembranous - metabolism</topic><topic>Enterocolitis, Pseudomembranous - microbiology</topic><topic>Enterocolitis, Pseudomembranous - prevention & control</topic><topic>Gene Expression Regulation</topic><topic>GPI-Linked Proteins - antagonists & inhibitors</topic><topic>GPI-Linked Proteins - genetics</topic><topic>GPI-Linked Proteins - immunology</topic><topic>GPI-Linked Proteins - metabolism</topic><topic>Immunity, Mucosal - drug effects</topic><topic>Interleukin-22</topic><topic>Interleukins - antagonists & inhibitors</topic><topic>Interleukins - genetics</topic><topic>Interleukins - immunology</topic><topic>Interleukins - metabolism</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Intestinal Mucosa - immunology</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - microbiology</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Neutrophil Infiltration</topic><topic>Original</topic><topic>Phosphorylation</topic><topic>pSTAT3</topic><topic>Receptors, Immunologic - antagonists & inhibitors</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - immunology</topic><topic>Receptors, Immunologic - metabolism</topic><topic>RegIIIγ</topic><topic>Signal Transduction</topic><topic>STAT3 Transcription Factor - immunology</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sadighi Akha, Amir A.</creatorcontrib><creatorcontrib>McDermott, Andrew J.</creatorcontrib><creatorcontrib>Theriot, Casey M.</creatorcontrib><creatorcontrib>Carlson, Paul E.</creatorcontrib><creatorcontrib>Frank, Charles R.</creatorcontrib><creatorcontrib>McDonald, Roderick A.</creatorcontrib><creatorcontrib>Falkowski, Nicole R.</creatorcontrib><creatorcontrib>Bergin, Ingrid L.</creatorcontrib><creatorcontrib>Young, Vincent B.</creatorcontrib><creatorcontrib>Huffnagle, Gary B.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Immunology 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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sadighi Akha, Amir A.</au><au>McDermott, Andrew J.</au><au>Theriot, Casey M.</au><au>Carlson, Paul E.</au><au>Frank, Charles R.</au><au>McDonald, Roderick A.</au><au>Falkowski, Nicole R.</au><au>Bergin, Ingrid L.</au><au>Young, Vincent B.</au><au>Huffnagle, Gary B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin‐22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice</atitle><jtitle>Immunology</jtitle><addtitle>Immunology</addtitle><date>2015-04</date><risdate>2015</risdate><volume>144</volume><issue>4</issue><spage>587</spage><epage>597</epage><pages>587-597</pages><issn>0019-2805</issn><eissn>1365-2567</eissn><abstract>Summary
Our previous work has shown the significant up‐regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes interleukin‐22 (IL‐22) and CD160‐mediated components. The current study sought to determine the potential role(s) of IL‐22 and/or CD160 in the mucosal response to C. difficile infection. Clostridium difficile‐infected mice treated with anti‐IL‐22, anti‐CD160 or a combination of the two showed significantly reduced STAT3 phosphorylation in comparison to C. difficile‐infected mice that had not received either antibody. In addition, C. difficile‐infected mice treated with anti‐IL‐22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile‐infected mice. The affected genes included pro‐inflammatory chemokines and cytokines, and anti‐microbial peptides. Furthermore, histopathological and flow cytometric assessments both showed a significantly reduced influx of neutrophils in C. difficile‐infected mice treated with anti‐IL‐22/CD160. These data demonstrate that IL‐22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL‐22 and CD160 in mediating both the pro‐inflammatory and pro‐survival aspects of the host mucosal response in this infection.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>25327211</pmid><doi>10.1111/imm.12414</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Bacterial Agents Antibodies - pharmacology Antigens, CD - genetics Antigens, CD - immunology Antigens, CD - metabolism CD160 Clostridioides difficile - immunology Clostridioides difficile - pathogenicity Clostridium difficile Disease Models, Animal Enterocolitis, Pseudomembranous - genetics Enterocolitis, Pseudomembranous - immunology Enterocolitis, Pseudomembranous - metabolism Enterocolitis, Pseudomembranous - microbiology Enterocolitis, Pseudomembranous - prevention & control Gene Expression Regulation GPI-Linked Proteins - antagonists & inhibitors GPI-Linked Proteins - genetics GPI-Linked Proteins - immunology GPI-Linked Proteins - metabolism Immunity, Mucosal - drug effects Interleukin-22 Interleukins - antagonists & inhibitors Interleukins - genetics Interleukins - immunology Interleukins - metabolism Intestinal Mucosa - drug effects Intestinal Mucosa - immunology Intestinal Mucosa - metabolism Intestinal Mucosa - microbiology Male Mice, Inbred C57BL Neutrophil Infiltration Original Phosphorylation pSTAT3 Receptors, Immunologic - antagonists & inhibitors Receptors, Immunologic - genetics Receptors, Immunologic - immunology Receptors, Immunologic - metabolism RegIIIγ Signal Transduction STAT3 Transcription Factor - immunology STAT3 Transcription Factor - metabolism Time Factors |
| title | Interleukin‐22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice |
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