Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted, interferongamma dependent, and toll-like receptor 4 independent
Mycoplasma arthritidis causes arthritis in rodents that resembles human rheumatoid arthritis. It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here...
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| Veröffentlicht in: | Experimental cell research 2003-06, Vol.286 (2), p.345-354 |
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| description | Mycoplasma arthritidis causes arthritis in rodents that resembles human rheumatoid arthritis. It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here we studied MAM-induced nitric oxide (NO) production in mouse peritoneal macrophages and found that it was: (1) time and concentration dependent, (2) possibly derived from inducible NOS synthase since it was reduced significantly by amino guanidine pretreatment, (3) restricted to H-2(K) (C3H/HePas and C3H/HeJ) and H-2(d) strains (BALB/c), (4) independent of TLR4 signaling since the coisogenic strains C3H/HePas and C3H/HeJ (TLR4 deficient) produced similar levels of NO following MAM stimulation, (5) potentiated by lipopolysaccharide, and (6) dependent on the presence of nonadherent peritoneal cells. Neutralization of interferon-gamma (IFNgamma in the peritoneal cell cultures with monoclonal antibodies abolished MAM-induced NO production. Addition of rIFNgamma to the adherent cells substituted the nonadherent cells for MAM-induced NO production. A macrophage cell line, J774A.1 (H-2(d)), also produced NO upon MAM stimulation but only when BALB/c spleen lymphocytes were added. Thus, in murine macrophages, MAM induces NO production that is dependent on signaling through MHC class II molecules and IFNgamma but independent of TLR4 expression. |
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It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here we studied MAM-induced nitric oxide (NO) production in mouse peritoneal macrophages and found that it was: (1) time and concentration dependent, (2) possibly derived from inducible NOS synthase since it was reduced significantly by amino guanidine pretreatment, (3) restricted to H-2(K) (C3H/HePas and C3H/HeJ) and H-2(d) strains (BALB/c), (4) independent of TLR4 signaling since the coisogenic strains C3H/HePas and C3H/HeJ (TLR4 deficient) produced similar levels of NO following MAM stimulation, (5) potentiated by lipopolysaccharide, and (6) dependent on the presence of nonadherent peritoneal cells. Neutralization of interferon-gamma (IFNgamma in the peritoneal cell cultures with monoclonal antibodies abolished MAM-induced NO production. Addition of rIFNgamma to the adherent cells substituted the nonadherent cells for MAM-induced NO production. A macrophage cell line, J774A.1 (H-2(d)), also produced NO upon MAM stimulation but only when BALB/c spleen lymphocytes were added. Thus, in murine macrophages, MAM induces NO production that is dependent on signaling through MHC class II molecules and IFNgamma but independent of TLR4 expression.</description><identifier>ISSN: 0014-4827</identifier><identifier>PMID: 12749862</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antigens ; Antigens, Bacterial ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - metabolism ; Cell Communication - immunology ; Cells, Cultured ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Histocompatibility Antigens Class II - drug effects ; Histocompatibility Antigens Class II - metabolism ; Interferon-gamma - metabolism ; Interferon-gamma - pharmacology ; Lymphocyte Activation - drug effects ; Lymphocyte Activation - immunology ; Lymphocytes - immunology ; Lymphocytes - metabolism ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Membrane Glycoproteins - drug effects ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mitogens - pharmacology ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - drug effects ; Nitric Oxide Synthase - metabolism ; Proteins ; Receptors, Cell Surface - drug effects ; Receptors, Cell Surface - metabolism ; Signal Transduction - drug effects ; Signal Transduction - immunology ; Superantigens ; Toll-Like Receptor 4 ; Toll-Like Receptors</subject><ispartof>Experimental cell research, 2003-06, Vol.286 (2), p.345-354</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12749862$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ribeiro-Dias, Fátima</creatorcontrib><creatorcontrib>Shio, Marina Tiemi</creatorcontrib><creatorcontrib>Timenetsky, Jorge</creatorcontrib><creatorcontrib>Oliane, Ana Paula Camilo</creatorcontrib><creatorcontrib>Metran, Camila Cardoso</creatorcontrib><creatorcontrib>Pessoa, Fábio Borges</creatorcontrib><creatorcontrib>Jancar, Sonia</creatorcontrib><title>Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted, interferongamma dependent, and toll-like receptor 4 independent</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>Mycoplasma arthritidis causes arthritis in rodents that resembles human rheumatoid arthritis. It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here we studied MAM-induced nitric oxide (NO) production in mouse peritoneal macrophages and found that it was: (1) time and concentration dependent, (2) possibly derived from inducible NOS synthase since it was reduced significantly by amino guanidine pretreatment, (3) restricted to H-2(K) (C3H/HePas and C3H/HeJ) and H-2(d) strains (BALB/c), (4) independent of TLR4 signaling since the coisogenic strains C3H/HePas and C3H/HeJ (TLR4 deficient) produced similar levels of NO following MAM stimulation, (5) potentiated by lipopolysaccharide, and (6) dependent on the presence of nonadherent peritoneal cells. Neutralization of interferon-gamma (IFNgamma in the peritoneal cell cultures with monoclonal antibodies abolished MAM-induced NO production. Addition of rIFNgamma to the adherent cells substituted the nonadherent cells for MAM-induced NO production. A macrophage cell line, J774A.1 (H-2(d)), also produced NO upon MAM stimulation but only when BALB/c spleen lymphocytes were added. Thus, in murine macrophages, MAM induces NO production that is dependent on signaling through MHC class II molecules and IFNgamma but independent of TLR4 expression.</description><subject>Animals</subject><subject>Antigens</subject><subject>Antigens, Bacterial</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Cell Communication - immunology</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Histocompatibility Antigens Class II - drug effects</subject><subject>Histocompatibility Antigens Class II - metabolism</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferon-gamma - pharmacology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Lymphocyte Activation - immunology</subject><subject>Lymphocytes - immunology</subject><subject>Lymphocytes - metabolism</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Membrane Glycoproteins - drug effects</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Mitogens - pharmacology</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - drug effects</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Proteins</subject><subject>Receptors, Cell Surface - drug effects</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - immunology</subject><subject>Superantigens</subject><subject>Toll-Like Receptor 4</subject><subject>Toll-Like Receptors</subject><issn>0014-4827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LAzEQhveg2Fr9C5KTKHQhm2w36bEUPwpdvPS-TJNpG80ma5IF-6P8j26xehoYnveZ4b3IxpQWZV5KJkbZdYzvlFIpi-oqGxVMlHNZsXH2XR-V7yzEFgiEdAgmGW0iiX2HAVwye3TkoV7Uj7lxuleoSQsq-O4AeyTOpGAU8V9GIwloESKSIV2_LokapJGsVsM-nqiEekqMSxh2GLzbQzuc1Nih0-jSlIDTJHlrc2s-TjKFXfKBlEPmn7rJLndgI96e5yTbPD9tlq_5-u1ltVys825Wslxw2FEuGAosqu2cVciYYFAxUVAJQgIVTCBDKIqt0EqUBWNqxqXe8gqlonyS3f9qu-A_--H9pjVRobXg0PexEZwzIaQcwLsz2G9b1E0XTAvh2Pz1y38Abud4gQ</recordid><startdate>20030610</startdate><enddate>20030610</enddate><creator>Ribeiro-Dias, Fátima</creator><creator>Shio, Marina Tiemi</creator><creator>Timenetsky, Jorge</creator><creator>Oliane, Ana Paula Camilo</creator><creator>Metran, Camila Cardoso</creator><creator>Pessoa, Fábio Borges</creator><creator>Jancar, Sonia</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20030610</creationdate><title>Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted, interferongamma dependent, and toll-like receptor 4 independent</title><author>Ribeiro-Dias, Fátima ; Shio, Marina Tiemi ; Timenetsky, Jorge ; Oliane, Ana Paula Camilo ; Metran, Camila Cardoso ; Pessoa, Fábio Borges ; Jancar, Sonia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p542-73af0372e7e16b926e2272a627108a78a0727e2ea11b7dc74122c538db36e8c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Antigens, Bacterial</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Cell Communication - immunology</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Histocompatibility Antigens Class II - drug effects</topic><topic>Histocompatibility Antigens Class II - metabolism</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferon-gamma - pharmacology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Lymphocyte Activation - immunology</topic><topic>Lymphocytes - immunology</topic><topic>Lymphocytes - metabolism</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Membrane Glycoproteins - drug effects</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Mitogens - pharmacology</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - drug effects</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Proteins</topic><topic>Receptors, Cell Surface - drug effects</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - immunology</topic><topic>Superantigens</topic><topic>Toll-Like Receptor 4</topic><topic>Toll-Like Receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ribeiro-Dias, Fátima</creatorcontrib><creatorcontrib>Shio, Marina Tiemi</creatorcontrib><creatorcontrib>Timenetsky, Jorge</creatorcontrib><creatorcontrib>Oliane, Ana Paula Camilo</creatorcontrib><creatorcontrib>Metran, Camila Cardoso</creatorcontrib><creatorcontrib>Pessoa, Fábio Borges</creatorcontrib><creatorcontrib>Jancar, Sonia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ribeiro-Dias, Fátima</au><au>Shio, Marina Tiemi</au><au>Timenetsky, Jorge</au><au>Oliane, Ana Paula Camilo</au><au>Metran, Camila Cardoso</au><au>Pessoa, Fábio Borges</au><au>Jancar, Sonia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted, interferongamma dependent, and toll-like receptor 4 independent</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>2003-06-10</date><risdate>2003</risdate><volume>286</volume><issue>2</issue><spage>345</spage><epage>354</epage><pages>345-354</pages><issn>0014-4827</issn><abstract>Mycoplasma arthritidis causes arthritis in rodents that resembles human rheumatoid arthritis. It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here we studied MAM-induced nitric oxide (NO) production in mouse peritoneal macrophages and found that it was: (1) time and concentration dependent, (2) possibly derived from inducible NOS synthase since it was reduced significantly by amino guanidine pretreatment, (3) restricted to H-2(K) (C3H/HePas and C3H/HeJ) and H-2(d) strains (BALB/c), (4) independent of TLR4 signaling since the coisogenic strains C3H/HePas and C3H/HeJ (TLR4 deficient) produced similar levels of NO following MAM stimulation, (5) potentiated by lipopolysaccharide, and (6) dependent on the presence of nonadherent peritoneal cells. Neutralization of interferon-gamma (IFNgamma in the peritoneal cell cultures with monoclonal antibodies abolished MAM-induced NO production. Addition of rIFNgamma to the adherent cells substituted the nonadherent cells for MAM-induced NO production. A macrophage cell line, J774A.1 (H-2(d)), also produced NO upon MAM stimulation but only when BALB/c spleen lymphocytes were added. Thus, in murine macrophages, MAM induces NO production that is dependent on signaling through MHC class II molecules and IFNgamma but independent of TLR4 expression.</abstract><cop>United States</cop><pmid>12749862</pmid><tpages>10</tpages></addata></record> |
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| ispartof | Experimental cell research, 2003-06, Vol.286 (2), p.345-354 |
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| subjects | Animals Antigens Antigens, Bacterial Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - metabolism Cell Communication - immunology Cells, Cultured Disease Models, Animal Dose-Response Relationship, Drug Histocompatibility Antigens Class II - drug effects Histocompatibility Antigens Class II - metabolism Interferon-gamma - metabolism Interferon-gamma - pharmacology Lymphocyte Activation - drug effects Lymphocyte Activation - immunology Lymphocytes - immunology Lymphocytes - metabolism Macrophages - drug effects Macrophages - metabolism Male Membrane Glycoproteins - drug effects Membrane Glycoproteins - metabolism Mice Mice, Inbred BALB C Mice, Inbred C3H Mice, Inbred C57BL Mitogens - pharmacology Nitric Oxide - biosynthesis Nitric Oxide Synthase - drug effects Nitric Oxide Synthase - metabolism Proteins Receptors, Cell Surface - drug effects Receptors, Cell Surface - metabolism Signal Transduction - drug effects Signal Transduction - immunology Superantigens Toll-Like Receptor 4 Toll-Like Receptors |
| title | Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted, interferongamma dependent, and toll-like receptor 4 independent |
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