Differential effects of interleukin-1α and β on the arachidonic acid cascade in human synovial cells and chondrocytes in culture

Isabelle Knott; Marc Dieu; Maggi Burton; Véronique Lecomte; José Remacle; Martine Raes

doi:10.1007/BF01998964

Differential effects of interleukin-1α and β on the arachidonic acid cascade in human synovial cells and chondrocytes in culture

Isabelle Knott, Marc Dieu, Maggi Burton, Véronique Lecomte, José Remacle, Martine Raes

Research output: Contribution to journal › Article › peer-review

Abstract

The effects of interleukin-1α and β were tested on the [³H]-arachidonic acid release and the prostaglandin synthesis by human cultured synovial cells and chondrocytes. Both forms of interleukin-1 stimulated the arachidonic acid release but interleukin-1α was more potent than IL-1β. Human synovial cells and chondrocytes synthesized three types of prostaglandins upon stimulation with interleukin-1α or β prostaglandin E₂, F(2α) and 6-keto-prostaglandin F(1α) Regarding the synthesis of these prostaglandins, IL-1β was again more potent than IL-1β. A comparison between interleukin-1-stimulated synovial cells a chondrocytes revealed neither significant quantitative nor qualitative differences in both the arachidonic acid release and the prostaglandin synthesis.

Original language	English
Pages (from-to)	126-131
Number of pages	6
Journal	Agents and Actions
Volume	39
Issue number	3-4
DOIs	https://doi.org/10.1007/BF01998964
Publication status	Published - 1993

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abstract = "The effects of interleukin-1α and β were tested on the [3H]-arachidonic acid release and the prostaglandin synthesis by human cultured synovial cells and chondrocytes. Both forms of interleukin-1 stimulated the arachidonic acid release but interleukin-1α was more potent than IL-1β. Human synovial cells and chondrocytes synthesized three types of prostaglandins upon stimulation with interleukin-1α or β prostaglandin E2, F(2α) and 6-keto-prostaglandin F(1α) Regarding the synthesis of these prostaglandins, IL-1β was again more potent than IL-1β. A comparison between interleukin-1-stimulated synovial cells a chondrocytes revealed neither significant quantitative nor qualitative differences in both the arachidonic acid release and the prostaglandin synthesis.",

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AU - Knott, Isabelle

AU - Dieu, Marc

AU - Burton, Maggi

AU - Lecomte, Véronique

AU - Remacle, José

AU - Raes, Martine

PY - 1993

Y1 - 1993

N2 - The effects of interleukin-1α and β were tested on the [3H]-arachidonic acid release and the prostaglandin synthesis by human cultured synovial cells and chondrocytes. Both forms of interleukin-1 stimulated the arachidonic acid release but interleukin-1α was more potent than IL-1β. Human synovial cells and chondrocytes synthesized three types of prostaglandins upon stimulation with interleukin-1α or β prostaglandin E2, F(2α) and 6-keto-prostaglandin F(1α) Regarding the synthesis of these prostaglandins, IL-1β was again more potent than IL-1β. A comparison between interleukin-1-stimulated synovial cells a chondrocytes revealed neither significant quantitative nor qualitative differences in both the arachidonic acid release and the prostaglandin synthesis.

AB - The effects of interleukin-1α and β were tested on the [3H]-arachidonic acid release and the prostaglandin synthesis by human cultured synovial cells and chondrocytes. Both forms of interleukin-1 stimulated the arachidonic acid release but interleukin-1α was more potent than IL-1β. Human synovial cells and chondrocytes synthesized three types of prostaglandins upon stimulation with interleukin-1α or β prostaglandin E2, F(2α) and 6-keto-prostaglandin F(1α) Regarding the synthesis of these prostaglandins, IL-1β was again more potent than IL-1β. A comparison between interleukin-1-stimulated synovial cells a chondrocytes revealed neither significant quantitative nor qualitative differences in both the arachidonic acid release and the prostaglandin synthesis.

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Differential effects of interleukin-1α and β on the arachidonic acid cascade in human synovial cells and chondrocytes in culture

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