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The cyclo‐oxygenase inhibitor, Piroxicam, enhances cytokine‐induced lymphocyte proliferation in vitro and in vivo
Author(s) -
Haynes D. R.,
Wright P. F.,
Whitehouse M. W.,
VerRoberts B.
Publication year - 1990
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1990.31
Subject(s) - piroxicam , in vivo , chemistry , pharmacology , in vitro , cytokine , lipopolysaccharide , immune system , peripheral blood mononuclear cell , prostaglandin e2 , ex vivo , immunology , endocrinology , biochemistry , medicine , biology , alternative medicine , microbiology and biotechnology , pathology
Summary The effects of Piroxicam on the production and activity of lymphoproliferative cytokines (LC) produced by mononuclear phagocytes (MNP) were examined. In vitro , Piroxicam did not affect IL‐1 induced thymocyte proliferation (LAF assay). However, the LAF activity from lipopolysaccharide (LPS)‐treated MNP cultures was increased after Piroxicam (0·1–20 μol/L) treatment. The increase in apparent LC activity was largely due to suppression of prostaglandin E 2 (PGE 2 ) production. Peripheral blood, spleen and thymus lymphocytes from animals predosed with Piroxicam (5 mg/kg per day for 3 days) synthesized more DNA than untreated mice (as measured by [ 3 H]‐thymidine uptake ex vivo ). MNP from Piroxicam‐treated animals produced significantly more LC. Piroxicam had similar effects in both inflamed and non‐inflamed mice. Piroxicam and other non‐steroidal anti‐inflammatory drugs (NSAID) may therefore stimulate or modulate the immune functions requiring lymphoproliferation by suppressing the formation of PGE 2 , a natural inhibitor of both LC production and LC‐induced lymphoproliferation.