Immune subversion by Mycobacterium tuberculosis through CCR5 mediated signaling: involvement of IL-10
Tuberculosis is characterized by severe immunosuppression of the host macrophages, resulting in the loss of the host protective immune responses. During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible i...
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| Veröffentlicht in: | PloS one 2014-04, Vol.9 (4), p.e92477-e92477 |
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| creator | Das, Shibali Banerjee, Sayantan Majumder, Saikat Chowdhury, Bidisha Paul Goswami, Avranil Halder, Kuntal Chakraborty, Urmita Pal, Nishith K Majumdar, Subrata |
| description | Tuberculosis is characterized by severe immunosuppression of the host macrophages, resulting in the loss of the host protective immune responses. During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible involvement of CCR5 in regulation of the host immune response. Here, we found that Mycobacterium infection significantly increased CCR5 expression in macrophages there by facilitating the activation of its downstream signaling. These events culminated in up-regulation of the immunosuppressive cytokine IL-10 production, which was further associated with the down-regulation of macrophage MHC-II expression along with the up-regulation of CCR5 expression via engagement of STAT-3 in a positive feedback loop. Treatment of macrophages with CCR5 specific siRNA abrogated the IL-10 production and restored MHCII expression. While, in vivo CCR5 silencing was also effective for the restoration of host immune responses against tuberculosis. This study demonstrated that CCR5 played a very critical role for the immune subversion mechanism employed by the pathogen. |
| doi_str_mv | 10.1371/journal.pone.0092477 |
| format | Article |
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During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible involvement of CCR5 in regulation of the host immune response. Here, we found that Mycobacterium infection significantly increased CCR5 expression in macrophages there by facilitating the activation of its downstream signaling. These events culminated in up-regulation of the immunosuppressive cytokine IL-10 production, which was further associated with the down-regulation of macrophage MHC-II expression along with the up-regulation of CCR5 expression via engagement of STAT-3 in a positive feedback loop. Treatment of macrophages with CCR5 specific siRNA abrogated the IL-10 production and restored MHCII expression. While, in vivo CCR5 silencing was also effective for the restoration of host immune responses against tuberculosis. This study demonstrated that CCR5 played a very critical role for the immune subversion mechanism employed by the pathogen.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0092477</identifier><identifier>PMID: 24695099</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Bacterial infections ; Biology and Life Sciences ; Bone marrow ; Carbon-carbon composites ; Causes of ; CCR5 protein ; Cell activation ; Chemokine receptors ; Chemokines ; Cytokines ; Development and progression ; Down-regulation ; Feedback loops ; Female ; Garra ; Gene Expression Regulation - immunology ; Genetic aspects ; Health aspects ; Health education ; Histocompatibility Antigens Class II - immunology ; HIV ; Human immunodeficiency virus ; Immune Evasion ; Immune response ; Immune system ; Immunosuppression ; Infections ; Interleukin 10 ; Interleukin-10 - immunology ; Laboratory animals ; Macrophages ; Macrophages - immunology ; Macrophages - microbiology ; Major histocompatibility complex ; Medicine ; Mice ; Mice, Inbred BALB C ; Mycobacterium ; Mycobacterium bovis ; Mycobacterium tuberculosis ; Mycobacterium tuberculosis - immunology ; Pathogens ; Physiological aspects ; Plasmids ; Positive feedback ; Receptors, CCR5 - immunology ; Regulations ; Restoration ; Signal Transduction - immunology ; Signaling ; siRNA ; Stat3 protein ; STAT3 Transcription Factor - immunology ; TNF inhibitors ; Tuberculosis ; Tuberculosis - immunology ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2014-04, Vol.9 (4), p.e92477-e92477</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Das et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Das et al 2014 Das et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-627512258ad98dcc0c21a8f9f874f88984669890b02daae863af4456bae4bce53</citedby><cites>FETCH-LOGICAL-c692t-627512258ad98dcc0c21a8f9f874f88984669890b02daae863af4456bae4bce53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973661/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973661/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24695099$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Das, Gobardhan</contributor><creatorcontrib>Das, Shibali</creatorcontrib><creatorcontrib>Banerjee, Sayantan</creatorcontrib><creatorcontrib>Majumder, Saikat</creatorcontrib><creatorcontrib>Chowdhury, Bidisha Paul</creatorcontrib><creatorcontrib>Goswami, Avranil</creatorcontrib><creatorcontrib>Halder, Kuntal</creatorcontrib><creatorcontrib>Chakraborty, Urmita</creatorcontrib><creatorcontrib>Pal, Nishith K</creatorcontrib><creatorcontrib>Majumdar, Subrata</creatorcontrib><title>Immune subversion by Mycobacterium tuberculosis through CCR5 mediated signaling: involvement of IL-10</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Tuberculosis is characterized by severe immunosuppression of the host macrophages, resulting in the loss of the host protective immune responses. During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible involvement of CCR5 in regulation of the host immune response. Here, we found that Mycobacterium infection significantly increased CCR5 expression in macrophages there by facilitating the activation of its downstream signaling. These events culminated in up-regulation of the immunosuppressive cytokine IL-10 production, which was further associated with the down-regulation of macrophage MHC-II expression along with the up-regulation of CCR5 expression via engagement of STAT-3 in a positive feedback loop. Treatment of macrophages with CCR5 specific siRNA abrogated the IL-10 production and restored MHCII expression. While, in vivo CCR5 silencing was also effective for the restoration of host immune responses against tuberculosis. This study demonstrated that CCR5 played a very critical role for the immune subversion mechanism employed by the pathogen.</description><subject>Animals</subject><subject>Bacterial infections</subject><subject>Biology and Life Sciences</subject><subject>Bone marrow</subject><subject>Carbon-carbon composites</subject><subject>Causes of</subject><subject>CCR5 protein</subject><subject>Cell activation</subject><subject>Chemokine receptors</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Down-regulation</subject><subject>Feedback loops</subject><subject>Female</subject><subject>Garra</subject><subject>Gene Expression Regulation - immunology</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Health education</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>HIV</subject><subject>Human immunodeficiency virus</subject><subject>Immune Evasion</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunosuppression</subject><subject>Infections</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - immunology</subject><subject>Laboratory animals</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - microbiology</subject><subject>Major histocompatibility complex</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mycobacterium</subject><subject>Mycobacterium bovis</subject><subject>Mycobacterium tuberculosis</subject><subject>Mycobacterium tuberculosis - immunology</subject><subject>Pathogens</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Positive feedback</subject><subject>Receptors, CCR5 - immunology</subject><subject>Regulations</subject><subject>Restoration</subject><subject>Signal Transduction - immunology</subject><subject>Signaling</subject><subject>siRNA</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - immunology</subject><subject>TNF inhibitors</subject><subject>Tuberculosis</subject><subject>Tuberculosis - immunology</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><sourceid>DOA</sourceid><recordid>eNqNk11r2zAUhs3YWLtu_2BshsHYLpJJ1pe1i0EJ-whkFLqPWyHLkqNgW6kkh-XfT2ncEo9eDF_ISM959Z6jc7LsJQRziBj8sHGD72U737pezwHgBWbsUXYOOSpmtADo8cn_WfYshA0ABJWUPs3OCkw5AZyfZ3rZdUOv8zBUO-2DdX1e7fPve-UqqaL2dujyOFTaq6F1wYY8rr0bmnW-WFyTvNO1lVHXebBN8mL75mNu-51rd7rTfcydyZerGQTPsydGtkG_GNeL7NeXzz8X32arq6_LxeVqpigvYrLKCCwKUsqal7VSQBVQloabkmFTlrzElPKSgwoUtZS6pEgajAmtpMaV0gRdZK-PuttkVowVCgImVQQZxjARyyNRO7kRW2876ffCSStuN5xvhPTRqlYLXklTg6qGGFCMpakIRkyRwmCGjJRV0vo03jZUqRIqZexlOxGdnvR2LRq3E4gzROnBzLtRwLubQYcoOhuUblvZazfc-kYAM0hZQt_8gz6c3Ug1MiVge-PSveogKi4RI6QsCDlQ8weo9NW6syq1k7FpfxLwfhKQmKj_xEYOIYjlj-v_Z69-T9m3J-xayzaug2uHmNowTEF8BJV3IXht7osMgThMw101xGEaxDgNKezV6QPdB921P_oLx4YE6w</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>Das, Shibali</creator><creator>Banerjee, Sayantan</creator><creator>Majumder, Saikat</creator><creator>Chowdhury, Bidisha Paul</creator><creator>Goswami, Avranil</creator><creator>Halder, Kuntal</creator><creator>Chakraborty, Urmita</creator><creator>Pal, Nishith K</creator><creator>Majumdar, Subrata</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140401</creationdate><title>Immune subversion by Mycobacterium tuberculosis through CCR5 mediated signaling: involvement of IL-10</title><author>Das, Shibali ; Banerjee, Sayantan ; Majumder, Saikat ; Chowdhury, Bidisha Paul ; Goswami, Avranil ; Halder, Kuntal ; Chakraborty, Urmita ; Pal, Nishith K ; Majumdar, Subrata</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-627512258ad98dcc0c21a8f9f874f88984669890b02daae863af4456bae4bce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Bacterial infections</topic><topic>Biology and Life Sciences</topic><topic>Bone marrow</topic><topic>Carbon-carbon composites</topic><topic>Causes of</topic><topic>CCR5 protein</topic><topic>Cell activation</topic><topic>Chemokine receptors</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Down-regulation</topic><topic>Feedback loops</topic><topic>Female</topic><topic>Garra</topic><topic>Gene Expression Regulation - immunology</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Health education</topic><topic>Histocompatibility Antigens Class II - immunology</topic><topic>HIV</topic><topic>Human immunodeficiency virus</topic><topic>Immune Evasion</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunosuppression</topic><topic>Infections</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - immunology</topic><topic>Laboratory animals</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - microbiology</topic><topic>Major histocompatibility complex</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mycobacterium</topic><topic>Mycobacterium bovis</topic><topic>Mycobacterium tuberculosis</topic><topic>Mycobacterium tuberculosis - immunology</topic><topic>Pathogens</topic><topic>Physiological aspects</topic><topic>Plasmids</topic><topic>Positive feedback</topic><topic>Receptors, CCR5 - 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During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible involvement of CCR5 in regulation of the host immune response. Here, we found that Mycobacterium infection significantly increased CCR5 expression in macrophages there by facilitating the activation of its downstream signaling. These events culminated in up-regulation of the immunosuppressive cytokine IL-10 production, which was further associated with the down-regulation of macrophage MHC-II expression along with the up-regulation of CCR5 expression via engagement of STAT-3 in a positive feedback loop. Treatment of macrophages with CCR5 specific siRNA abrogated the IL-10 production and restored MHCII expression. While, in vivo CCR5 silencing was also effective for the restoration of host immune responses against tuberculosis. This study demonstrated that CCR5 played a very critical role for the immune subversion mechanism employed by the pathogen.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24695099</pmid><doi>10.1371/journal.pone.0092477</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-04, Vol.9 (4), p.e92477-e92477 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1512317441 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Bacterial infections Biology and Life Sciences Bone marrow Carbon-carbon composites Causes of CCR5 protein Cell activation Chemokine receptors Chemokines Cytokines Development and progression Down-regulation Feedback loops Female Garra Gene Expression Regulation - immunology Genetic aspects Health aspects Health education Histocompatibility Antigens Class II - immunology HIV Human immunodeficiency virus Immune Evasion Immune response Immune system Immunosuppression Infections Interleukin 10 Interleukin-10 - immunology Laboratory animals Macrophages Macrophages - immunology Macrophages - microbiology Major histocompatibility complex Medicine Mice Mice, Inbred BALB C Mycobacterium Mycobacterium bovis Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology Pathogens Physiological aspects Plasmids Positive feedback Receptors, CCR5 - immunology Regulations Restoration Signal Transduction - immunology Signaling siRNA Stat3 protein STAT3 Transcription Factor - immunology TNF inhibitors Tuberculosis Tuberculosis - immunology Tumor necrosis factor-TNF |
| title | Immune subversion by Mycobacterium tuberculosis through CCR5 mediated signaling: involvement of IL-10 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T03%3A06%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Immune%20subversion%20by%20Mycobacterium%20tuberculosis%20through%20CCR5%20mediated%20signaling:%20involvement%20of%20IL-10&rft.jtitle=PloS%20one&rft.au=Das,%20Shibali&rft.date=2014-04-01&rft.volume=9&rft.issue=4&rft.spage=e92477&rft.epage=e92477&rft.pages=e92477-e92477&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0092477&rft_dat=%3Cgale_plos_%3EA375582551%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1512317441&rft_id=info:pmid/24695099&rft_galeid=A375582551&rft_doaj_id=oai_doaj_org_article_9bafd0bd140644afb5437c52f473faab&rfr_iscdi=true |