Pharmacology of human spontaneous monocyte‐mediated cytotoxicity

E. S. Kleinerman; J. S. Louie; L. M. Wahl; A. V. Muchmore

doi:10.1002/art.1780240604

Pharmacology of human spontaneous monocyte‐mediated cytotoxicity

E. S. Kleinerman, J. S. Louie, L. M. Wahl, A. V. Muchmore

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5 Scopus citations

Abstract

The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte‐mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE₂ to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which has no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte‐mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.

Original language	English (US)
Pages (from-to)	774-780
Number of pages	7
Journal	Arthritis & Rheumatism
Volume	24
Issue number	6
DOIs	https://doi.org/10.1002/art.1780240604
State	Published - Jun 1981
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Rheumatology
Immunology
Pharmacology (medical)

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10.1002/art.1780240604

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abstract = "The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte‐mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE2 to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which has no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte‐mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.",

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AU - Kleinerman, E. S.

AU - Louie, J. S.

AU - Wahl, L. M.

AU - Muchmore, A. V.

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N2 - The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte‐mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE2 to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which has no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte‐mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.

AB - The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte‐mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE2 to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which has no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte‐mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.

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Pharmacology of human spontaneous monocyte‐mediated cytotoxicity

Abstract

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