Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage
The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey “pocket” model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5lex) into subcutaneous pockets containing salpingeal au...
Gespeichert in:
| Veröffentlicht in: | The Journal of infectious diseases 1994-03, Vol.169 (3), p.680-685 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 685 |
|---|---|
| container_issue | 3 |
| container_start_page | 680 |
| container_title | The Journal of infectious diseases |
| container_volume | 169 |
| creator | Patton, Dorothy L. Cosgrove Sweeney, Yvonne T. Kuo, Cho-Chou |
| description | The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey “pocket” model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5lex) into subcutaneous pockets containing salpingeal autotransplants. At 21 days, affinity-purified recombinant C. trachomatis heat-shock protein (rhsp60) wasinjected into pockets either previouslysensitizedwith C. trachomatis or not sensitized in the same monkey. Delayed-type hypersensitivity reaction was observed, characterized bymononuclear cell infiltration with peak reaction at 48 h. Injection of rhsp60 into the pockets of a naive animal did not induce inflammation. This study showed that C. trachomatis infection in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delayed hypersensitivity reaction observed in ocular C. trachomatis infection, further suggesting a similar pathogenesis for both salpingitis and trachoma. |
| doi_str_mv | 10.1093/infdis/169.3.680 |
| format | Article |
| fullrecord | <record><control><sourceid>jstor_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_76445628</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>30113802</jstor_id><sourcerecordid>30113802</sourcerecordid><originalsourceid>FETCH-LOGICAL-c416t-575e4ae05e3dcfcdb99322ee75e6541201feb76e3f782aa1c707bbaef6612f0a3</originalsourceid><addsrcrecordid>eNqFkcFv0zAUxiMEGmVw54LkA-KW7jlOnITb1AJF2sSkDYS4WC_Oc-stcTo7ReTIf46rlnLkZMu_7_ue9b4kec1hzqEWF9aZ1oYLLuu5mMsKniQzXogylZKLp8kMIMtSXtX18-RFCPcAkAtZniVnFS8qKPgs-b2kfnBh9DjawbHBsCV1OFHLVtOWfCAX7Gh_2nFi1rHFpsN-ai2yaNCboY-uwG6x21q3tvt7FF0P7oGm8J5dshscN8OanNXsmvQGnQ39fsbdrsGOLbHHNb1MnhnsAr06nufJ148f7har9OrLp8-Ly6tU51yOaVEWlCNBQaLVRrdNXYssI4rPssh5BtxQU0oSpqwyRK5LKJsGycRVZAZQnCfvDrlbPzzuKIyqt0FT16GjYRdUKfO8kFn1X2FctgRRFlEIB6H2QwiejNp626OfFAe1r0cd6tk7lFCxnmh5c8zeNT21J8Oxj8jfHjkGjZ3x6HQM-CvLoZJ1nf-LuQ_j4E9YAOeigizy9MBtGOnXiaN_ULKMX1er7z9U_Q1ubuvrparEH4uhtJU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>16960375</pqid></control><display><type>article</type><title>Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage</title><source>Jstor Complete Legacy</source><source>MEDLINE</source><creator>Patton, Dorothy L. ; Cosgrove Sweeney, Yvonne T. ; Kuo, Cho-Chou</creator><creatorcontrib>Patton, Dorothy L. ; Cosgrove Sweeney, Yvonne T. ; Kuo, Cho-Chou</creatorcontrib><description>The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey “pocket” model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5lex) into subcutaneous pockets containing salpingeal autotransplants. At 21 days, affinity-purified recombinant C. trachomatis heat-shock protein (rhsp60) wasinjected into pockets either previouslysensitizedwith C. trachomatis or not sensitized in the same monkey. Delayed-type hypersensitivity reaction was observed, characterized bymononuclear cell infiltration with peak reaction at 48 h. Injection of rhsp60 into the pockets of a naive animal did not induce inflammation. This study showed that C. trachomatis infection in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delayed hypersensitivity reaction observed in ocular C. trachomatis infection, further suggesting a similar pathogenesis for both salpingitis and trachoma.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/169.3.680</identifier><identifier>PMID: 8158051</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>Animals ; Antigens ; Autologous transplantation ; Bacterial diseases ; Biological and medical sciences ; Chlamydia ; Chlamydia Infections - immunology ; Chlamydia trachomatis ; Chlamydia trachomatis - immunology ; Concise Communications ; Delayed hypersensitivity ; Experimental bacterial diseases and models ; Fallopian Tubes - transplantation ; Female ; HeLa Cells ; Humans ; Hypersensitivity, Delayed - immunology ; Infections ; Infectious diseases ; Inoculation ; Macaca nemestrina ; Medical sciences ; Pathogenesis ; Salpingitis ; Salpingitis - immunology ; Salpingitis - microbiology ; Trachoma</subject><ispartof>The Journal of infectious diseases, 1994-03, Vol.169 (3), p.680-685</ispartof><rights>Copyright 1994 The University of Chicago</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-575e4ae05e3dcfcdb99322ee75e6541201feb76e3f782aa1c707bbaef6612f0a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30113802$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30113802$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4086994$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8158051$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Patton, Dorothy L.</creatorcontrib><creatorcontrib>Cosgrove Sweeney, Yvonne T.</creatorcontrib><creatorcontrib>Kuo, Cho-Chou</creatorcontrib><title>Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey “pocket” model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5lex) into subcutaneous pockets containing salpingeal autotransplants. At 21 days, affinity-purified recombinant C. trachomatis heat-shock protein (rhsp60) wasinjected into pockets either previouslysensitizedwith C. trachomatis or not sensitized in the same monkey. Delayed-type hypersensitivity reaction was observed, characterized bymononuclear cell infiltration with peak reaction at 48 h. Injection of rhsp60 into the pockets of a naive animal did not induce inflammation. This study showed that C. trachomatis infection in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delayed hypersensitivity reaction observed in ocular C. trachomatis infection, further suggesting a similar pathogenesis for both salpingitis and trachoma.</description><subject>Animals</subject><subject>Antigens</subject><subject>Autologous transplantation</subject><subject>Bacterial diseases</subject><subject>Biological and medical sciences</subject><subject>Chlamydia</subject><subject>Chlamydia Infections - immunology</subject><subject>Chlamydia trachomatis</subject><subject>Chlamydia trachomatis - immunology</subject><subject>Concise Communications</subject><subject>Delayed hypersensitivity</subject><subject>Experimental bacterial diseases and models</subject><subject>Fallopian Tubes - transplantation</subject><subject>Female</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Hypersensitivity, Delayed - immunology</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Inoculation</subject><subject>Macaca nemestrina</subject><subject>Medical sciences</subject><subject>Pathogenesis</subject><subject>Salpingitis</subject><subject>Salpingitis - immunology</subject><subject>Salpingitis - microbiology</subject><subject>Trachoma</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFv0zAUxiMEGmVw54LkA-KW7jlOnITb1AJF2sSkDYS4WC_Oc-stcTo7ReTIf46rlnLkZMu_7_ue9b4kec1hzqEWF9aZ1oYLLuu5mMsKniQzXogylZKLp8kMIMtSXtX18-RFCPcAkAtZniVnFS8qKPgs-b2kfnBh9DjawbHBsCV1OFHLVtOWfCAX7Gh_2nFi1rHFpsN-ai2yaNCboY-uwG6x21q3tvt7FF0P7oGm8J5dshscN8OanNXsmvQGnQ39fsbdrsGOLbHHNb1MnhnsAr06nufJ148f7har9OrLp8-Ly6tU51yOaVEWlCNBQaLVRrdNXYssI4rPssh5BtxQU0oSpqwyRK5LKJsGycRVZAZQnCfvDrlbPzzuKIyqt0FT16GjYRdUKfO8kFn1X2FctgRRFlEIB6H2QwiejNp626OfFAe1r0cd6tk7lFCxnmh5c8zeNT21J8Oxj8jfHjkGjZ3x6HQM-CvLoZJ1nf-LuQ_j4E9YAOeigizy9MBtGOnXiaN_ULKMX1er7z9U_Q1ubuvrparEH4uhtJU</recordid><startdate>19940301</startdate><enddate>19940301</enddate><creator>Patton, Dorothy L.</creator><creator>Cosgrove Sweeney, Yvonne T.</creator><creator>Kuo, Cho-Chou</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><scope>BSCLL</scope><scope>IQODW</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>C1K</scope><scope>7X8</scope></search><sort><creationdate>19940301</creationdate><title>Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage</title><author>Patton, Dorothy L. ; Cosgrove Sweeney, Yvonne T. ; Kuo, Cho-Chou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-575e4ae05e3dcfcdb99322ee75e6541201feb76e3f782aa1c707bbaef6612f0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Autologous transplantation</topic><topic>Bacterial diseases</topic><topic>Biological and medical sciences</topic><topic>Chlamydia</topic><topic>Chlamydia Infections - immunology</topic><topic>Chlamydia trachomatis</topic><topic>Chlamydia trachomatis - immunology</topic><topic>Concise Communications</topic><topic>Delayed hypersensitivity</topic><topic>Experimental bacterial diseases and models</topic><topic>Fallopian Tubes - transplantation</topic><topic>Female</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Hypersensitivity, Delayed - immunology</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Inoculation</topic><topic>Macaca nemestrina</topic><topic>Medical sciences</topic><topic>Pathogenesis</topic><topic>Salpingitis</topic><topic>Salpingitis - immunology</topic><topic>Salpingitis - microbiology</topic><topic>Trachoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patton, Dorothy L.</creatorcontrib><creatorcontrib>Cosgrove Sweeney, Yvonne T.</creatorcontrib><creatorcontrib>Kuo, Cho-Chou</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</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>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patton, Dorothy L.</au><au>Cosgrove Sweeney, Yvonne T.</au><au>Kuo, Cho-Chou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>1994-03-01</date><risdate>1994</risdate><volume>169</volume><issue>3</issue><spage>680</spage><epage>685</epage><pages>680-685</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey “pocket” model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5lex) into subcutaneous pockets containing salpingeal autotransplants. At 21 days, affinity-purified recombinant C. trachomatis heat-shock protein (rhsp60) wasinjected into pockets either previouslysensitizedwith C. trachomatis or not sensitized in the same monkey. Delayed-type hypersensitivity reaction was observed, characterized bymononuclear cell infiltration with peak reaction at 48 h. Injection of rhsp60 into the pockets of a naive animal did not induce inflammation. This study showed that C. trachomatis infection in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delayed hypersensitivity reaction observed in ocular C. trachomatis infection, further suggesting a similar pathogenesis for both salpingitis and trachoma.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>8158051</pmid><doi>10.1093/infdis/169.3.680</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-1899 |
| ispartof | The Journal of infectious diseases, 1994-03, Vol.169 (3), p.680-685 |
| issn | 0022-1899 1537-6613 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_76445628 |
| source | Jstor Complete Legacy; MEDLINE |
| subjects | Animals Antigens Autologous transplantation Bacterial diseases Biological and medical sciences Chlamydia Chlamydia Infections - immunology Chlamydia trachomatis Chlamydia trachomatis - immunology Concise Communications Delayed hypersensitivity Experimental bacterial diseases and models Fallopian Tubes - transplantation Female HeLa Cells Humans Hypersensitivity, Delayed - immunology Infections Infectious diseases Inoculation Macaca nemestrina Medical sciences Pathogenesis Salpingitis Salpingitis - immunology Salpingitis - microbiology Trachoma |
| title | Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T09%3A33%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Demonstration%20of%20Delayed%20Hypersensitivity%20in%20Chlamydia%20trachomatis%20Salpingitis%20in%20Monkeys:%20A%20Pathogenic%20Mechanism%20of%20Tubal%20Damage&rft.jtitle=The%20Journal%20of%20infectious%20diseases&rft.au=Patton,%20Dorothy%20L.&rft.date=1994-03-01&rft.volume=169&rft.issue=3&rft.spage=680&rft.epage=685&rft.pages=680-685&rft.issn=0022-1899&rft.eissn=1537-6613&rft.coden=JIDIAQ&rft_id=info:doi/10.1093/infdis/169.3.680&rft_dat=%3Cjstor_proqu%3E30113802%3C/jstor_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=16960375&rft_id=info:pmid/8158051&rft_jstor_id=30113802&rfr_iscdi=true |