Augmentation of concanavalin A-induced immunosuppression by indomethacin |
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| Authors: | A M Badger D E Griswold D T Walz |
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| Affiliation: | 1. School of Materials Science and Engineering, Chongqing University, Chongqing, 400044, China;2. International Joint Laboratory for Light Alloys, College of Materials Science and Engineering, Chongqing University, Chongqing, 400030, China;3. School of Materials Science and Engineering, Jiangsu University of Science and Technology, Zhenjiang, 212003, China;4. State Key Laboratory of Powder Metallurgy, Central South University, Changsha, 410083, China;1. Instituto de Ciencias Matemáticas (ICMAT) and Departamento de Matemáticas, Universidad Carlos III de Madrid, Avenida de la Universidad 30, 28911 Leganés, Spain;2. Department of Mathematics, University of Oregon, Eugene OR 97403-1222, United States;1. Department of Pharmacy – Pharmaceutical Sciences, University of Bari “Aldo Moro”, 70125 Bari, Italy;2. Department of Pharmaceutical Technology, University of Innsbruck, Institute of Pharmacy, Center for Chemistry and Biomedicine, 6020 Innsbruck, Austria;3. Faculty of Pharmaceutical Sciences, University of Iceland, Reykjavik, Iceland;1. Division of Biochemistry, School of Life Science, JSS Academy of Higher Education and Research, Mysore-15, India;2. Department of Biochemistry, Adichunchanagiri Institute of Medical Sciences, Adichunchanagiri University, B. G. Nagara- 571448, Nagamangala (T), Mandya (D), Karnataka, India;3. Department of Biotechnology, Adichunchanagiri School of Natural Sciences, ACU-CRI, Adichunchanagiri University, B. G. Nagara- 571448, Nagamangala (T), Mandya (D), Karnataka, India;4. Department of Biotechnology & Bioinformatics, JSS Academy of Higher Education & Research, Mysore-15, India;5. Department of Microbiology, School of Life Sciences, JSS Academy of Higher Education and Research, Mysore-15, India;6. Department of Biotechnology, Sri Jayachamarajendra College of Engineering, JSS Science and Technological University, Mysore, India;7. Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Mysore-15, India;1. Department of Materials Science and Engineering, The Pennsylvania State University, University Park, PA 16802, USA;2. National Energy Technology Laboratory, Morgantown, WV 26507, USA |
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| Abstract: | These studies show that, in BALB/C mice, when antibody synthesis against sheep red blood cells is suppressed by concanavalin A, treatment with indomethacin (4-8 mg/kg per os) will augment this suppression. Two other nonsteroidal anti-inflammatory drugs, flufenamic acid and meclofenamic acid (50 mg/kg), also have this effect, whereas phenylbutazone was inactive at this dose. The augmentation of concanavalin A-induced immunosuppression by indomethacin could not be demonstrated on the response to the T-independent antigen polyvinypyrrolidone. In contrast to indomethacin, which inhibits cyclooxygenase, neither nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway, nor eicosa-5,8,11,14-tetraynoic acid, an inhibitor of both the cyclooxygenase and the lipoxygenase pathways, had this augmenting effect. Therefore, we do not have strong evidence that the absence of a prostaglandin is responsible for the effect of indomethacin. However, inhibition of the pathway leading to prostaglandin synthesis causes an increase in arachidonic acid metabolism via the lipoxygenase pathway. A product of this pathway, such as a leukotriene, may have immunosuppressive effects in this model. Evidence for the enhancement of a suppressor cell population is provided by an in vitro coculture assay. Cells treated with concanavalin A and indomethacin had more suppressive activity than cells treated with concanavalin A or indomethacin alone. |
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