Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ
The proinflammatory cytokine interleukin (IL)-17 plays important roles in various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have received much attention. For therapy of Th17-mediated diseases, some reports have indicated the clinical efficacy of lactic acid bacteria, includ...
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| Veröffentlicht in: | International journal of molecular medicine 2011-11, Vol.28 (5), p.817-822 |
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| container_title | International journal of molecular medicine |
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| creator | Ogita, Tasuku Tanii, Yusuke Morita, Hidetoshi Suzuki, Takuya Tanabe, Soichi |
| description | The proinflammatory cytokine interleukin (IL)-17 plays important roles in
various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have
received much attention. For therapy of Th17-mediated diseases, some reports have
indicated the clinical efficacy of lactic acid bacteria, including Streptococcus
thermophilus. In this study, we examined the mechanism for the suppressive effects
of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated
with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus
IL-6 increased mRNA expression of IL-17 and its production in the splenocytes,
but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression
of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled
the suppressive effect of ST28 on IL-17 production. From these data, it was concluded
that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA
(10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the
Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of
the mechanisms under which S. thermophilus ST28 exerts an anti-inflammatory effect. |
| doi_str_mv | 10.3892/ijmm.2011.755 |
| format | Article |
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various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have
received much attention. For therapy of Th17-mediated diseases, some reports have
indicated the clinical efficacy of lactic acid bacteria, including Streptococcus
thermophilus. In this study, we examined the mechanism for the suppressive effects
of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated
with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus
IL-6 increased mRNA expression of IL-17 and its production in the splenocytes,
but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression
of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled
the suppressive effect of ST28 on IL-17 production. From these data, it was concluded
that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA
(10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the
Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of
the mechanisms under which S. thermophilus ST28 exerts an anti-inflammatory effect.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2011.755</identifier><identifier>PMID: 21887477</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Female ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-17 - genetics ; Interleukin-17 - metabolism ; Interleukin-6 - pharmacology ; Mice ; Mice, Inbred BALB C ; Streptococcus thermophilus - immunology ; Transforming Growth Factor beta - pharmacology</subject><ispartof>International journal of molecular medicine, 2011-11, Vol.28 (5), p.817-822</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c367t-a6397ed068bc45ba466015cb7205f40b968d8d6179ebb7cead4b02d5c012fe93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21887477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ogita, Tasuku</creatorcontrib><creatorcontrib>Tanii, Yusuke</creatorcontrib><creatorcontrib>Morita, Hidetoshi</creatorcontrib><creatorcontrib>Suzuki, Takuya</creatorcontrib><creatorcontrib>Tanabe, Soichi</creatorcontrib><title>Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>The proinflammatory cytokine interleukin (IL)-17 plays important roles in
various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have
received much attention. For therapy of Th17-mediated diseases, some reports have
indicated the clinical efficacy of lactic acid bacteria, including Streptococcus
thermophilus. In this study, we examined the mechanism for the suppressive effects
of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated
with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus
IL-6 increased mRNA expression of IL-17 and its production in the splenocytes,
but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression
of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled
the suppressive effect of ST28 on IL-17 production. From these data, it was concluded
that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA
(10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the
Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of
the mechanisms under which S. thermophilus ST28 exerts an anti-inflammatory effect.</description><subject>Animals</subject><subject>Female</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-6 - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Streptococcus thermophilus - immunology</subject><subject>Transforming Growth Factor beta - pharmacology</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkLtOwzAUhi0EoqUwsqLsKMV2fMuIKgqVKhiaAYkhii8hqZrYspOhz8V78Ey4KoXpnP_o0y-dD4BbBOeZyPFDu-26OYYIzTmlZ2CKeI5STMj7edwR5GnGKZuAqxC2EGJKcnEJJhgJwQnnU_CxGZ3zJoTW9omtk6JBPInZ2T6YRO6TzeCNG6yySo0hGRrjO-uadhfDpsAiXrwdP5uk7fWoht-W1fI1_f66Bhd1tQvm5nfOQLF8KhYv6frtebV4XKcqY3xIK5bl3GjIhFSEyoowBhFVkmNIawJlzoQWmsXHjJRcmUoTCbGmCiJcmzybgfRYq7wNwZu6dL7tKr8vESwPjsqDo_LgqIyOIn935N0oO6P_6JOUCNwfgeCqXrfahv_Gk1EsqEBcYJz9AC4tcaE</recordid><startdate>20111101</startdate><enddate>20111101</enddate><creator>Ogita, Tasuku</creator><creator>Tanii, Yusuke</creator><creator>Morita, Hidetoshi</creator><creator>Suzuki, Takuya</creator><creator>Tanabe, Soichi</creator><general>D.A. Spandidos</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></search><sort><creationdate>20111101</creationdate><title>Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ</title><author>Ogita, Tasuku ; Tanii, Yusuke ; Morita, Hidetoshi ; Suzuki, Takuya ; Tanabe, Soichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c367t-a6397ed068bc45ba466015cb7205f40b968d8d6179ebb7cead4b02d5c012fe93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Female</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - metabolism</topic><topic>Interleukin-6 - pharmacology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Streptococcus thermophilus - immunology</topic><topic>Transforming Growth Factor beta - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ogita, Tasuku</creatorcontrib><creatorcontrib>Tanii, Yusuke</creatorcontrib><creatorcontrib>Morita, Hidetoshi</creatorcontrib><creatorcontrib>Suzuki, Takuya</creatorcontrib><creatorcontrib>Tanabe, Soichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ogita, Tasuku</au><au>Tanii, Yusuke</au><au>Morita, Hidetoshi</au><au>Suzuki, Takuya</au><au>Tanabe, Soichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2011-11-01</date><risdate>2011</risdate><volume>28</volume><issue>5</issue><spage>817</spage><epage>822</epage><pages>817-822</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>The proinflammatory cytokine interleukin (IL)-17 plays important roles in
various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have
received much attention. For therapy of Th17-mediated diseases, some reports have
indicated the clinical efficacy of lactic acid bacteria, including Streptococcus
thermophilus. In this study, we examined the mechanism for the suppressive effects
of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated
with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus
IL-6 increased mRNA expression of IL-17 and its production in the splenocytes,
but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression
of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled
the suppressive effect of ST28 on IL-17 production. From these data, it was concluded
that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA
(10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the
Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of
the mechanisms under which S. thermophilus ST28 exerts an anti-inflammatory effect.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>21887477</pmid><doi>10.3892/ijmm.2011.755</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Female Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-17 - genetics Interleukin-17 - metabolism Interleukin-6 - pharmacology Mice Mice, Inbred BALB C Streptococcus thermophilus - immunology Transforming Growth Factor beta - pharmacology |
| title | Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ |
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