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• W2097517368 abstract "Background:Cyclosporin A (CsA) binds with high affinity to cyclophilin, a critical step in the molecular mechanism of action of cyclosporins, whereas cyclosporin H (CsH) has extremely low affinity for cyclophilin. CsH differs from CsA by the substitution of the L-methyl valine at position 11 with its D-isomer. Methods: We compared the effects of CsA and CsH on the release of preformed (histamine) and de novo synthesized inflammatory mediators (peptide leukotriene C 4) from peripheral blood basophils activated by N-formyl-methionyl-leucyl-phenylalanine (FMLP). Results: CsH (8 to 800 nmol/L) concentration-dependently inhibited histamine and leukotriene C 4 release from purified and unpurified basophils activated by FMLP, whereas CsA (8 to 800 nmol/L) had little inhibitory effect on histamine release from basophils challenged with FMLP. Inhibition of histamine release from basophils challenged with FMLP was extremely rapid and was abolished by washing the cells (three times) before challenge. CsH (8 to 800 nmol/L) had no effect on the release of histamine caused by C5a, platelet activating factor, monocyte chemotactic activating factor, RANTES, IL-8, bryostatin 1, and phorbol myristate. Preincubation of basophils with granulocyte-macrophage colony-stimulating factor (30 and 100 pmol/L), but not IL-1β (30 and 100 ng/ml), concentration-dependently reversed the inhibitory effect of CsH on FMLP-induced histamine release. CsH competitively inhibited the effect of FMLP on histamine release from basophils. The dissociation constant (K d) for the CsH-FMLP receptor complex was approximately 9 × 10-8 mol/L, more than 10-fold lower than that (≅ 1.3 × 10-6 mol/L) of N-t-BOC-methionyl-L-leucyl-phenylalanine (BocMLP), a known formyl peptide receptor antagonist. CsH inhibited tritiated FMLP binding to human polymorphonuclear leukocytes with a concentration required to inhibit binding by 50% of approximately 5.4 × 10-7 mol/L, whereas BocMLP was less potent with a concentration required to inhibit binding by 50% of approximately 9.1 × 10-5 mol/L. Scatchard analysis revealed that the decreased tritiated FMLP binding caused by CsH was due to a decrease in the B max (0.22 ± 0.04 nmol/L/5 × 106 cells vs 0.09 ± 0.01 nmol/L/5 × 106 cells; p < 0.05), without a significant difference in the K d (5.16 ± 1.22 nmol/L vs 6.32 ± 2.42 nmol/L; p = NS). Conclusions: CsH is a potent and selective inhibitor of mediator release from basophils induced by activation of the formyl peptide receptor; it acts by interfering with agonist binding to FMLP receptors. (J ALLERGY CLIN IMMUNOL 1996;98:152-64.)" @default.
• W2097517368 created "2016-06-24" @default.
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• W2097517368 date "1996-07-01" @default.
• W2097517368 modified "2023-09-26" @default.
• W2097517368 title "Cyclosporin H is a potent and selective competitive antagonist of human basophil activation by N-formyl-methionyl-leucyl-phenylalanine☆, ☆☆, ★, ★★" @default.
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• W2097517368 doi "https://doi.org/10.1016/s0091-6749(96)70237-3" @default.
• W2097517368 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8765829" @default.
• W2097517368 hasPublicationYear "1996" @default.
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