Induction of CXC Chemokine Messenger-RNA Expression in Chicken Oviduct Epithelial Cells by Salmonella enterica Serovar Enteritidis via the Type Three Secretion System–1
The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infections with wild-type or type three secretion system (T3SS)–mutant Salmonella enterica serovar Enteritidis (SE) strains. All SE strains ex...
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| Veröffentlicht in: | Avian diseases 2009-09, Vol.53 (3), p.396-404 |
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| creator | Li, Shuhui Zhang, M. Zhenyu Yan, Lifang Lillehoj, Hyun Pace, Lanny W Zhang, Shuping |
| description | The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infections with wild-type or type three secretion system (T3SS)–mutant Salmonella enterica serovar Enteritidis (SE) strains. All SE strains examined in this study elicited the expression of proinflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1β). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-β3 transcription. Both T3SS-1 (sipA and sipB) and T3SS-2 (pipB and ssaV) mutants showed reduced capacity, compared to the wild-type SE, to stimulate iNOS mRNA expression in COEC. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild-type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. The expression of iNOS, but not CXC chemokines, correlated with the number of intracellular bacteria in COEC. Genetic complementation of the sipA mutation restored a wild-type phenotype. Thus, SE induction of CXCLi1 and CXCLi2 was sipA-dependent. These results provide enhanced insights into the complex interplay between local host innate immune system and bacterial virulence factors. |
| doi_str_mv | 10.1637/8642-020309-Reg.1 |
| format | Article |
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Zhenyu ; Yan, Lifang ; Lillehoj, Hyun ; Pace, Lanny W ; Zhang, Shuping</creator><creatorcontrib>Li, Shuhui ; Zhang, M. Zhenyu ; Yan, Lifang ; Lillehoj, Hyun ; Pace, Lanny W ; Zhang, Shuping</creatorcontrib><description>The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infections with wild-type or type three secretion system (T3SS)–mutant Salmonella enterica serovar Enteritidis (SE) strains. All SE strains examined in this study elicited the expression of proinflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1β). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-β3 transcription. Both T3SS-1 (sipA and sipB) and T3SS-2 (pipB and ssaV) mutants showed reduced capacity, compared to the wild-type SE, to stimulate iNOS mRNA expression in COEC. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild-type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. The expression of iNOS, but not CXC chemokines, correlated with the number of intracellular bacteria in COEC. Genetic complementation of the sipA mutation restored a wild-type phenotype. Thus, SE induction of CXCLi1 and CXCLi2 was sipA-dependent. These results provide enhanced insights into the complex interplay between local host innate immune system and bacterial virulence factors.</description><identifier>ISSN: 0005-2086</identifier><identifier>EISSN: 1938-4351</identifier><identifier>DOI: 10.1637/8642-020309-Reg.1</identifier><identifier>PMID: 19848079</identifier><language>eng</language><publisher>United States: American Association of Avian Pathologists</publisher><subject>animal pathogenic bacteria ; Animals ; Bacteria ; Bacterial Proteins - pharmacology ; Cell Death ; Cells, Cultured ; Chemokines ; Chemokines, CXC - genetics ; Chemokines, CXC - metabolism ; Chickens ; CXC chemokines ; Cytokines ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - microbiology ; Female ; gene expression ; Gene Expression Regulation - physiology ; genetic complementation ; immune response ; immune system ; in vitro studies ; Infections ; inflammation ; interleukin-10 ; Messenger RNA ; Microfilament Proteins - pharmacology ; mutants ; nitric oxide synthase ; oviduct epithelial cells ; oviducts ; Oviducts - cytology ; phenotype ; Regular s ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Salmonella ; Salmonella enterica ; Salmonella enteritidis ; Salmonella enteritidis - physiology ; salmonellosis ; Secretory Pathway ; Time Factors ; transcription (genetics) ; transforming growth factor beta ; Type III secretion system ; virulence</subject><ispartof>Avian diseases, 2009-09, Vol.53 (3), p.396-404</ispartof><rights>American Association of Avian Pathologists</rights><rights>Copyright 2009 The American Association of Avian Pathologists, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b515t-b9b89805579b3e2c20b31251001b5b7031a8f2a0c4fa54785f29acc555f87ab13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://bioone.org/doi/pdf/10.1637/8642-020309-Reg.1$$EPDF$$P50$$Gbioone$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25599131$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,26957,27903,27904,52341,57995,58228</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19848079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shuhui</creatorcontrib><creatorcontrib>Zhang, M. Zhenyu</creatorcontrib><creatorcontrib>Yan, Lifang</creatorcontrib><creatorcontrib>Lillehoj, Hyun</creatorcontrib><creatorcontrib>Pace, Lanny W</creatorcontrib><creatorcontrib>Zhang, Shuping</creatorcontrib><title>Induction of CXC Chemokine Messenger-RNA Expression in Chicken Oviduct Epithelial Cells by Salmonella enterica Serovar Enteritidis via the Type Three Secretion System–1</title><title>Avian diseases</title><addtitle>Avian Dis</addtitle><description>The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infections with wild-type or type three secretion system (T3SS)–mutant Salmonella enterica serovar Enteritidis (SE) strains. All SE strains examined in this study elicited the expression of proinflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1β). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-β3 transcription. Both T3SS-1 (sipA and sipB) and T3SS-2 (pipB and ssaV) mutants showed reduced capacity, compared to the wild-type SE, to stimulate iNOS mRNA expression in COEC. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild-type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. The expression of iNOS, but not CXC chemokines, correlated with the number of intracellular bacteria in COEC. Genetic complementation of the sipA mutation restored a wild-type phenotype. Thus, SE induction of CXCLi1 and CXCLi2 was sipA-dependent. These results provide enhanced insights into the complex interplay between local host innate immune system and bacterial virulence factors.</description><subject>animal pathogenic bacteria</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial Proteins - pharmacology</subject><subject>Cell Death</subject><subject>Cells, Cultured</subject><subject>Chemokines</subject><subject>Chemokines, CXC - genetics</subject><subject>Chemokines, CXC - metabolism</subject><subject>Chickens</subject><subject>CXC chemokines</subject><subject>Cytokines</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - microbiology</subject><subject>Female</subject><subject>gene expression</subject><subject>Gene Expression Regulation - physiology</subject><subject>genetic complementation</subject><subject>immune response</subject><subject>immune system</subject><subject>in vitro studies</subject><subject>Infections</subject><subject>inflammation</subject><subject>interleukin-10</subject><subject>Messenger RNA</subject><subject>Microfilament Proteins - pharmacology</subject><subject>mutants</subject><subject>nitric oxide synthase</subject><subject>oviduct epithelial cells</subject><subject>oviducts</subject><subject>Oviducts - cytology</subject><subject>phenotype</subject><subject>Regular s</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Salmonella</subject><subject>Salmonella enterica</subject><subject>Salmonella enteritidis</subject><subject>Salmonella enteritidis - physiology</subject><subject>salmonellosis</subject><subject>Secretory Pathway</subject><subject>Time Factors</subject><subject>transcription (genetics)</subject><subject>transforming growth factor beta</subject><subject>Type III secretion system</subject><subject>virulence</subject><issn>0005-2086</issn><issn>1938-4351</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQxi0EokvhATgAPsEprf_EiX2sogUqFSp1W4mbZWcnu26TeGtnV-yNd-AteCyeBKdZwQ24eOSZ33z6Rh9CLyk5oQUvT2WRs4wwwonKrmB1Qh-hGVVcZjkX9DGaEUJExogsjtCzGG8JoaUqyFN0RJXMJSnVDP0475fbenC-x77B1ZcKV2vo_J3rAX-CGKFfQciuPp_h-ddNSI2RdH2iXH0HPb7cuXEfzzduWEPrTIsraNuI7R4vTNv5Pv0Mhn6A4GqDFxD8zgQ8f2gMbuki3jmD0zK-3m_Ssw4ACasDPLha7OMA3c9v3-lz9KQxbYQXh3qMbt7Pr6uP2cXlh_Pq7CKzgoohs8pKJYkQpbIcWM2I5ZQJmq63wpaEUyMbZkidN0bkpRQNU6auhRCNLI2l_Bi9m3Q3wd9vIQ66c7Eez-jBb6OWJaOcMCr_TXJVSEmVSOTbv5JFWaics1GSTmAdfIwBGr0JrjNhrynRY-h6DF1PoesUuh4Nvz6Ib20Hyz8bh5QT8GoCbuPgw-85E0IpykeBN9O8MV6bVXBR3ywYSVfSQpU5Gf2fToR1PkX6H6Z-ASJZy2Y</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Li, Shuhui</creator><creator>Zhang, M. Zhenyu</creator><creator>Yan, Lifang</creator><creator>Lillehoj, Hyun</creator><creator>Pace, Lanny W</creator><creator>Zhang, Shuping</creator><general>American Association of Avian Pathologists</general><scope>FBQ</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>7X8</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>20090901</creationdate><title>Induction of CXC Chemokine Messenger-RNA Expression in Chicken Oviduct Epithelial Cells by Salmonella enterica Serovar Enteritidis via the Type Three Secretion System–1</title><author>Li, Shuhui ; Zhang, M. Zhenyu ; Yan, Lifang ; Lillehoj, Hyun ; Pace, Lanny W ; Zhang, Shuping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b515t-b9b89805579b3e2c20b31251001b5b7031a8f2a0c4fa54785f29acc555f87ab13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>animal pathogenic bacteria</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Bacterial Proteins - pharmacology</topic><topic>Cell Death</topic><topic>Cells, Cultured</topic><topic>Chemokines</topic><topic>Chemokines, CXC - genetics</topic><topic>Chemokines, CXC - metabolism</topic><topic>Chickens</topic><topic>CXC chemokines</topic><topic>Cytokines</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - microbiology</topic><topic>Female</topic><topic>gene expression</topic><topic>Gene Expression Regulation - physiology</topic><topic>genetic complementation</topic><topic>immune response</topic><topic>immune system</topic><topic>in vitro studies</topic><topic>Infections</topic><topic>inflammation</topic><topic>interleukin-10</topic><topic>Messenger RNA</topic><topic>Microfilament Proteins - pharmacology</topic><topic>mutants</topic><topic>nitric oxide synthase</topic><topic>oviduct epithelial cells</topic><topic>oviducts</topic><topic>Oviducts - cytology</topic><topic>phenotype</topic><topic>Regular s</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Salmonella</topic><topic>Salmonella enterica</topic><topic>Salmonella enteritidis</topic><topic>Salmonella enteritidis - physiology</topic><topic>salmonellosis</topic><topic>Secretory Pathway</topic><topic>Time Factors</topic><topic>transcription (genetics)</topic><topic>transforming growth factor beta</topic><topic>Type III secretion system</topic><topic>virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shuhui</creatorcontrib><creatorcontrib>Zhang, M. Zhenyu</creatorcontrib><creatorcontrib>Yan, Lifang</creatorcontrib><creatorcontrib>Lillehoj, Hyun</creatorcontrib><creatorcontrib>Pace, Lanny W</creatorcontrib><creatorcontrib>Zhang, Shuping</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Avian diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shuhui</au><au>Zhang, M. Zhenyu</au><au>Yan, Lifang</au><au>Lillehoj, Hyun</au><au>Pace, Lanny W</au><au>Zhang, Shuping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of CXC Chemokine Messenger-RNA Expression in Chicken Oviduct Epithelial Cells by Salmonella enterica Serovar Enteritidis via the Type Three Secretion System–1</atitle><jtitle>Avian diseases</jtitle><addtitle>Avian Dis</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>53</volume><issue>3</issue><spage>396</spage><epage>404</epage><pages>396-404</pages><issn>0005-2086</issn><eissn>1938-4351</eissn><abstract>The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infections with wild-type or type three secretion system (T3SS)–mutant Salmonella enterica serovar Enteritidis (SE) strains. All SE strains examined in this study elicited the expression of proinflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1β). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-β3 transcription. Both T3SS-1 (sipA and sipB) and T3SS-2 (pipB and ssaV) mutants showed reduced capacity, compared to the wild-type SE, to stimulate iNOS mRNA expression in COEC. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild-type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. The expression of iNOS, but not CXC chemokines, correlated with the number of intracellular bacteria in COEC. Genetic complementation of the sipA mutation restored a wild-type phenotype. Thus, SE induction of CXCLi1 and CXCLi2 was sipA-dependent. These results provide enhanced insights into the complex interplay between local host innate immune system and bacterial virulence factors.</abstract><cop>United States</cop><pub>American Association of Avian Pathologists</pub><pmid>19848079</pmid><doi>10.1637/8642-020309-Reg.1</doi><tpages>9</tpages></addata></record> |
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| subjects | animal pathogenic bacteria Animals Bacteria Bacterial Proteins - pharmacology Cell Death Cells, Cultured Chemokines Chemokines, CXC - genetics Chemokines, CXC - metabolism Chickens CXC chemokines Cytokines Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - microbiology Female gene expression Gene Expression Regulation - physiology genetic complementation immune response immune system in vitro studies Infections inflammation interleukin-10 Messenger RNA Microfilament Proteins - pharmacology mutants nitric oxide synthase oviduct epithelial cells oviducts Oviducts - cytology phenotype Regular s RNA, Messenger - genetics RNA, Messenger - metabolism Salmonella Salmonella enterica Salmonella enteritidis Salmonella enteritidis - physiology salmonellosis Secretory Pathway Time Factors transcription (genetics) transforming growth factor beta Type III secretion system virulence |
| title | Induction of CXC Chemokine Messenger-RNA Expression in Chicken Oviduct Epithelial Cells by Salmonella enterica Serovar Enteritidis via the Type Three Secretion System–1 |
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