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Nimesulide, a sulfonanilide nonsteroidal anti-inflammatory drug, inhibits mediator release from human basophils and mast cells.
J Pharmacol Exp Ther. 1993 Dec; 267(3):1375-85.JP

Abstract

Nimesulide (NIM) is a sulfonanilide nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of various inflammatory diseases and chemically unrelated to other acidic NSAIDs, such as acetylsalicylic acid (ASA) and indomethacin (INDO). We investigated the effects of NIM and of its in vivo metabolite, 4-hydroxy-NIM (OH-NIM), on the release of performed (histamine) and de novo synthesized mediators (sulfidopeptide leukotriene C4 [LTC4] and prostaglandin D2 [PGD2]) from human basophils and mast cells isolated from lung parenchyma (HLMC) and skin (HSMC). Histamine release from basophils challenged with rabbit anti-human IgE antibody (anti-IgE) was enhanced by preincubation with ASA or INDO (92.2 +/- 7.1% at 10(-3) M and 61.1 +/- 6.7% at 3 x 10(-6) M, respectively; P < .001). In contrast, NIM and its metabolite, OH-NIM (10(-6) to 10(-3) M), caused concentration-dependent inhibition (2.9 to approximately 60% and 3.7 to approximately 90%, respectively) of IgE-mediated histamine release from basophils. NIM and OH-NIM also inhibited histamine release from basophils induced by the Ca++ ionophore A23187 and different protein kinase C activators, such as 12-O-tetradecanoyl-phorbol-13-acetate, bryostatin 1 and bryostatin 5. NIM and OH-NIM also inhibited the IgE-mediated histamine release from HLMC (52.3 +/- 9.6% and 66.1 +/- 12.1% at 10(-3) M, respectively; P < .0001) and HSMC (67.3 +/- 3.7% and 77.7 +/- 12.0% at 10(-3) M, respectively; P < .0001) but had little or no effect on HLMC and HSMC activated by A23187. NIM (10(-6) to 10(-3) M) markedly inhibited the de novo synthesis of LTC4 from basophils, LTC4 and PGD2 from HLMC and PGD2 from HSMC. NIM and OH-NIM potentiated, whereas ASA and INDO reversed, the inhibitory effect of adenylate cyclase agonists, such as prostaglandin E1 and forskolin. In addition, NIM and OH-NIM reversed the enhancing effects of ASA and INDO on IgE-mediated histamine release from basophils.

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Authors+Show Affiliations

Casolaro V
Division of Clinical Immunology and Allergy, University of Naples Federico II School of Medicine, Italy.
Meliota S
No affiliation info available
Marino O
No affiliation info available
Patella V
No affiliation info available
de Paulis A
No affiliation info available
Guidi G
No affiliation info available
Marone G
No affiliation info available

MeSH

AdolescentAdultAlprostadilAmino Acid SequenceAnti-Inflammatory Agents, Non-SteroidalAspirinBasophilsBryostatinsCalcimycinColforsinComplement C5aHistamine ReleaseHumansImmunoglobulin EIndomethacinLactonesLeukotriene C4LungMacrolidesMast CellsMiddle AgedMolecular Sequence DataN-Formylmethionine Leucyl-PhenylalanineProstaglandin D2SkinSulfonamidesTetradecanoylphorbol Acetate

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7505332

Citation

Casolaro, V, et al. "Nimesulide, a Sulfonanilide Nonsteroidal Anti-inflammatory Drug, Inhibits Mediator Release From Human Basophils and Mast Cells." The Journal of Pharmacology and Experimental Therapeutics, vol. 267, no. 3, 1993, pp. 1375-85.
Casolaro V, Meliota S, Marino O, et al. Nimesulide, a sulfonanilide nonsteroidal anti-inflammatory drug, inhibits mediator release from human basophils and mast cells. J Pharmacol Exp Ther. 1993;267(3):1375-85.
Casolaro, V., Meliota, S., Marino, O., Patella, V., de Paulis, A., Guidi, G., & Marone, G. (1993). Nimesulide, a sulfonanilide nonsteroidal anti-inflammatory drug, inhibits mediator release from human basophils and mast cells. The Journal of Pharmacology and Experimental Therapeutics, 267(3), 1375-85.
Casolaro V, et al. Nimesulide, a Sulfonanilide Nonsteroidal Anti-inflammatory Drug, Inhibits Mediator Release From Human Basophils and Mast Cells. J Pharmacol Exp Ther. 1993;267(3):1375-85. PubMed PMID: 7505332.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nimesulide, a sulfonanilide nonsteroidal anti-inflammatory drug, inhibits mediator release from human basophils and mast cells. AU - Casolaro,V, AU - Meliota,S, AU - Marino,O, AU - Patella,V, AU - de Paulis,A, AU - Guidi,G, AU - Marone,G, PY - 1993/12/1/pubmed PY - 1993/12/1/medline PY - 1993/12/1/entrez SP - 1375 EP - 85 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 267 IS - 3 N2 - Nimesulide (NIM) is a sulfonanilide nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of various inflammatory diseases and chemically unrelated to other acidic NSAIDs, such as acetylsalicylic acid (ASA) and indomethacin (INDO). We investigated the effects of NIM and of its in vivo metabolite, 4-hydroxy-NIM (OH-NIM), on the release of performed (histamine) and de novo synthesized mediators (sulfidopeptide leukotriene C4 [LTC4] and prostaglandin D2 [PGD2]) from human basophils and mast cells isolated from lung parenchyma (HLMC) and skin (HSMC). Histamine release from basophils challenged with rabbit anti-human IgE antibody (anti-IgE) was enhanced by preincubation with ASA or INDO (92.2 +/- 7.1% at 10(-3) M and 61.1 +/- 6.7% at 3 x 10(-6) M, respectively; P < .001). In contrast, NIM and its metabolite, OH-NIM (10(-6) to 10(-3) M), caused concentration-dependent inhibition (2.9 to approximately 60% and 3.7 to approximately 90%, respectively) of IgE-mediated histamine release from basophils. NIM and OH-NIM also inhibited histamine release from basophils induced by the Ca++ ionophore A23187 and different protein kinase C activators, such as 12-O-tetradecanoyl-phorbol-13-acetate, bryostatin 1 and bryostatin 5. NIM and OH-NIM also inhibited the IgE-mediated histamine release from HLMC (52.3 +/- 9.6% and 66.1 +/- 12.1% at 10(-3) M, respectively; P < .0001) and HSMC (67.3 +/- 3.7% and 77.7 +/- 12.0% at 10(-3) M, respectively; P < .0001) but had little or no effect on HLMC and HSMC activated by A23187. NIM (10(-6) to 10(-3) M) markedly inhibited the de novo synthesis of LTC4 from basophils, LTC4 and PGD2 from HLMC and PGD2 from HSMC. NIM and OH-NIM potentiated, whereas ASA and INDO reversed, the inhibitory effect of adenylate cyclase agonists, such as prostaglandin E1 and forskolin. In addition, NIM and OH-NIM reversed the enhancing effects of ASA and INDO on IgE-mediated histamine release from basophils. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/7505332/Nimesulide_a_sulfonanilide_nonsteroidal_anti_inflammatory_drug_inhibits_mediator_release_from_human_basophils_and_mast_cells_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&amp;pmid=7505332 DB - PRIME DP - Unbound Medicine ER -