Dysregulation of adenosine A1 receptor–mediated cytokine expression in peripheral blood mononuclear cells from multiple sclerosis patients
Identifieur interne : 003766 ( Main/Exploration ); précédent : 003765; suivant : 003767Dysregulation of adenosine A1 receptor–mediated cytokine expression in peripheral blood mononuclear cells from multiple sclerosis patients
Auteurs : M. Mayne [Canada] ; P. N. Shepel [Canada] ; Y. Jiang [Canada] ; J. D. Geiger [Canada] ; C. Power [Canada]Source :
- Annals of Neurology [ 0364-5134 ] ; 1999-05.
Abstract
Cytokines, including tumor necrosis factor‐α (TNFα) and interleukin‐6 (IL‐6), have been implicated in the pathogenesis of multiple sclerosis (MS). The production and release of these cytokines are regulated in part by specific purinergic (adenosine) cell surface receptors. To determine the extent to which the adenosine A1 receptor influenced cytokine expression in peripheral blood mononuclear cells (PBMCs) from MS and control patients, we measured plasma adenosine and TNFα levels, A1 receptor messenger RNA (mRNA) and protein amounts, and the effects of activation of A1 receptors on TNFα and IL‐6 production by PBMCs. Plasma levels of TNFα were significantly higher and adenosine levels were significantly lower in MS patients compared with control subjects. Levels of TNFα and IL‐6 in mitogen‐stimulated PBMC culture supernatants from MS patients or control patients were similar. Conversely, treatment of PBMCs with the adenosine A1 receptor agonist R‐phenylisopropyladenosine (R‐PIA) (1 μM) significantly inhibited mitogen‐stimulated production of TNFα but not IL‐6 in control subjects and significantly inhibited production of IL‐6 but not TNFα in MS patients. The effects of R‐PIA were selectively blocked by the A1 receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX). A1 receptor protein levels were decreased significantly in PBMCs from MS patients. Taken together, these results suggest that decreased levels of adenosine and its A1 receptor modulate TNFα and IL‐6 levels and may contribute to the pathogenesis of MS. Ann Neurol 1999;45:633–639
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DOI: 10.1002/1531-8249(199905)45:5<633::AID-ANA12>3.0.CO;2-X
Affiliations:
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Mayne</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Shepel, P N" sort="Shepel, P N" uniqKey="Shepel P" first="P. N." last="Shepel">P. N. Shepel</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Jiang, Y" sort="Jiang, Y" uniqKey="Jiang Y" first="Y." last="Jiang">Y. Jiang</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, University of Manitoba, Winnipeg, Manitoba</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J. D." last="Geiger">J. D. Geiger</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Power, C" sort="Power, C" uniqKey="Power C" first="C." last="Power">C. Power</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, University of Calgary, 107‐3330 Hospital Drive, Calgary, Alberta T2N 4N1</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1999-05">1999-05</date><biblScope unit="volume">45</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="633">633</biblScope><biblScope unit="page" to="639">639</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">E13798DD2B79CB808026B1006A4E4D0CF80C4D0B</idno><idno type="DOI">10.1002/1531-8249(199905)45:5<633::AID-ANA12>3.0.CO;2-X</idno><idno type="ArticleID">ANA12</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cytokines, including tumor necrosis factor‐α (TNFα) and interleukin‐6 (IL‐6), have been implicated in the pathogenesis of multiple sclerosis (MS). The production and release of these cytokines are regulated in part by specific purinergic (adenosine) cell surface receptors. To determine the extent to which the adenosine A1 receptor influenced cytokine expression in peripheral blood mononuclear cells (PBMCs) from MS and control patients, we measured plasma adenosine and TNFα levels, A1 receptor messenger RNA (mRNA) and protein amounts, and the effects of activation of A1 receptors on TNFα and IL‐6 production by PBMCs. Plasma levels of TNFα were significantly higher and adenosine levels were significantly lower in MS patients compared with control subjects. Levels of TNFα and IL‐6 in mitogen‐stimulated PBMC culture supernatants from MS patients or control patients were similar. Conversely, treatment of PBMCs with the adenosine A1 receptor agonist R‐phenylisopropyladenosine (R‐PIA) (1 μM) significantly inhibited mitogen‐stimulated production of TNFα but not IL‐6 in control subjects and significantly inhibited production of IL‐6 but not TNFα in MS patients. The effects of R‐PIA were selectively blocked by the A1 receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX). A1 receptor protein levels were decreased significantly in PBMCs from MS patients. Taken together, these results suggest that decreased levels of adenosine and its A1 receptor modulate TNFα and IL‐6 levels and may contribute to the pathogenesis of MS. Ann Neurol 1999;45:633–639</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Alberta</li><li>Manitoba</li></region><settlement><li>Calgary</li><li>Winnipeg</li></settlement><orgName><li>Université de Calgary</li><li>Université du Manitoba</li></orgName></list><tree><country name="Canada"><region name="Manitoba"><name sortKey="Mayne, M" sort="Mayne, M" uniqKey="Mayne M" first="M." last="Mayne">M. Mayne</name></region><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J. D." last="Geiger">J. D. Geiger</name><name sortKey="Jiang, Y" sort="Jiang, Y" uniqKey="Jiang Y" first="Y." last="Jiang">Y. Jiang</name><name sortKey="Power, C" sort="Power, C" uniqKey="Power C" first="C." last="Power">C. Power</name><name sortKey="Power, C" sort="Power, C" uniqKey="Power C" first="C." last="Power">C. Power</name><name sortKey="Power, C" sort="Power, C" uniqKey="Power C" first="C." last="Power">C. Power</name><name sortKey="Shepel, P N" sort="Shepel, P N" uniqKey="Shepel P" first="P. N." last="Shepel">P. N. Shepel</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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