The augmentation of lymphokine-activated killer cell activity by indomethacin in vitro is not mediated by prostaglandin E2 suppression.

T. Y. Chao, C. S. Ting, T. M. Chu, M. Y. Yeh

Research output: Contribution to journalArticle

Abstract

The effects of three nonsteroidal antiinflammatory drugs (NSAIDs), namely, indomethacin, aspirin, and mefenamate (ponstan), on the lymphokine-activated killer (LAK) cell activities generated from coculturing recombinant interleukin-2 (rIL-2) and normal human peripheral blood mononuclear cells (PBMCs) for 3 to 4 days were investigated. The LAK cell activities were measured by a 4 hour 51Cr release microcytotoxicity assay using HL-60 and K-562 as target cells. Indomethacin was found to have significant augmenting effect on LAK cell activity at the concentration of 5 x 10(-5) M, whereas aspirin and ponstan did not show the same effect at the same concentration. Additional experiments, however, demonstrated that all of these 3 agents could effectively suppress the production of prostaglandin E2 (PGE2) in the culture medium. These results indicated that PGE2 suppression may not be the only mechanism of indomethacin for upregulation of LAK cell activity, and even immune functions.

Original languageEnglish
Pages (from-to)138-142
Number of pages5
JournalProceedings of the National Science Council, Republic of China. Part B, Life sciences
Volume17
Issue number4
Publication statusPublished - Oct 1993
Externally publishedYes

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Lymphokine-Activated Killer Cells
Dinoprostone
Indomethacin
Mefenamic Acid
Aspirin
Interleukin-2
Culture Media
Blood Cells
Anti-Inflammatory Agents
Up-Regulation
In Vitro Techniques
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "The augmentation of lymphokine-activated killer cell activity by indomethacin in vitro is not mediated by prostaglandin E2 suppression.",
abstract = "The effects of three nonsteroidal antiinflammatory drugs (NSAIDs), namely, indomethacin, aspirin, and mefenamate (ponstan), on the lymphokine-activated killer (LAK) cell activities generated from coculturing recombinant interleukin-2 (rIL-2) and normal human peripheral blood mononuclear cells (PBMCs) for 3 to 4 days were investigated. The LAK cell activities were measured by a 4 hour 51Cr release microcytotoxicity assay using HL-60 and K-562 as target cells. Indomethacin was found to have significant augmenting effect on LAK cell activity at the concentration of 5 x 10(-5) M, whereas aspirin and ponstan did not show the same effect at the same concentration. Additional experiments, however, demonstrated that all of these 3 agents could effectively suppress the production of prostaglandin E2 (PGE2) in the culture medium. These results indicated that PGE2 suppression may not be the only mechanism of indomethacin for upregulation of LAK cell activity, and even immune functions.",
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TY - JOUR

T1 - The augmentation of lymphokine-activated killer cell activity by indomethacin in vitro is not mediated by prostaglandin E2 suppression.

AU - Chao, T. Y.

AU - Ting, C. S.

AU - Chu, T. M.

AU - Yeh, M. Y.

PY - 1993/10

Y1 - 1993/10

N2 - The effects of three nonsteroidal antiinflammatory drugs (NSAIDs), namely, indomethacin, aspirin, and mefenamate (ponstan), on the lymphokine-activated killer (LAK) cell activities generated from coculturing recombinant interleukin-2 (rIL-2) and normal human peripheral blood mononuclear cells (PBMCs) for 3 to 4 days were investigated. The LAK cell activities were measured by a 4 hour 51Cr release microcytotoxicity assay using HL-60 and K-562 as target cells. Indomethacin was found to have significant augmenting effect on LAK cell activity at the concentration of 5 x 10(-5) M, whereas aspirin and ponstan did not show the same effect at the same concentration. Additional experiments, however, demonstrated that all of these 3 agents could effectively suppress the production of prostaglandin E2 (PGE2) in the culture medium. These results indicated that PGE2 suppression may not be the only mechanism of indomethacin for upregulation of LAK cell activity, and even immune functions.

AB - The effects of three nonsteroidal antiinflammatory drugs (NSAIDs), namely, indomethacin, aspirin, and mefenamate (ponstan), on the lymphokine-activated killer (LAK) cell activities generated from coculturing recombinant interleukin-2 (rIL-2) and normal human peripheral blood mononuclear cells (PBMCs) for 3 to 4 days were investigated. The LAK cell activities were measured by a 4 hour 51Cr release microcytotoxicity assay using HL-60 and K-562 as target cells. Indomethacin was found to have significant augmenting effect on LAK cell activity at the concentration of 5 x 10(-5) M, whereas aspirin and ponstan did not show the same effect at the same concentration. Additional experiments, however, demonstrated that all of these 3 agents could effectively suppress the production of prostaglandin E2 (PGE2) in the culture medium. These results indicated that PGE2 suppression may not be the only mechanism of indomethacin for upregulation of LAK cell activity, and even immune functions.

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