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Regulation of the synthesis and release of slow-reacting substance of anaphylaxis from sensitized monkey lung.
J Pharmacol Exp Ther. 1982 May; 221(2):295-302.JP

Abstract

Immunological challenge of sensitized fragmented cynomolgus monkey lung with anti-human IgE (immunoglobulin E) induced the appearance of slow reacting substance of anaphylaxis (SRS-A) in the tissue and evoked the release of SRS-A into the Tyrode's supernatant. The elevation of tissue or residual SRS-A levels was maximal 2 min after anti-IgE challenge and remained at that plateau for at least 60 min. The released SRS-A, first detectable 3 to 5 min after challenge, achieved a plateau by 10 min. Both the released and residual SRS-A were similarly inactivated by soybean lipoxidase and were antagonized by FPL 55712 on the guinea-pig ileum. Isoproterenol, 5, 8, 11, 14-eicosatraynoic acid and SK & F 64398 all inhibited the anti-IgE induced elevation in residual SRS-A and blocked SRS-A release. Indomethacin stimulated both the elevation of residual SRS-A and the amount released. Removal of the Tyrode's supernatant containing 209 +/- 73 U of released SRS-A/g of tissue 20 min after anti-IgE resulted in the release of an additional 239 +/- 69 U/g; residual SRS-A levels remained at the plateau level. Incubation of the Tyrode's supernatant from challenged, but not control, tissue with fresh lung tissue caused a 90 +/- 7% inhibition of SRS-A release from the fresh tissue. Leukotriene D4 at 5 to 50 ng/ml (concentrations relevant to SRS-A release) showed a concentration-dependent inhibition of SRS-A release, but no effect on histamine release. Leukotriene C4 at 5 to 50 ng/mg failed to significantly alter the amount of SRS-A release. However, at 150 ng/ml, significant inhibition was observed which, in part, may have been produced by metabolism to leukotriene D4. These results demonstrate a potential role for LTD in regulating the amount of SRS-A released from monkey lung.

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Authors

Weichman BM
No affiliation info available
Hostelley LS
No affiliation info available
Bostick SP
No affiliation info available
Muccitelli RM
No affiliation info available
Krell RD
No affiliation info available
Gleason JG
No affiliation info available

MeSH

AnimalsAnti-Inflammatory AgentsAntigensHistamine AntagonistsHistamine ReleaseLungMacaca fascicularisMaleSRS-ATime Factors

Pub Type(s)

Journal Article

Language

eng

PubMed ID

6176708

Citation

Weichman, B M., et al. "Regulation of the Synthesis and Release of Slow-reacting Substance of Anaphylaxis From Sensitized Monkey Lung." The Journal of Pharmacology and Experimental Therapeutics, vol. 221, no. 2, 1982, pp. 295-302.
Weichman BM, Hostelley LS, Bostick SP, et al. Regulation of the synthesis and release of slow-reacting substance of anaphylaxis from sensitized monkey lung. J Pharmacol Exp Ther. 1982;221(2):295-302.
Weichman, B. M., Hostelley, L. S., Bostick, S. P., Muccitelli, R. M., Krell, R. D., & Gleason, J. G. (1982). Regulation of the synthesis and release of slow-reacting substance of anaphylaxis from sensitized monkey lung. The Journal of Pharmacology and Experimental Therapeutics, 221(2), 295-302.
Weichman BM, et al. Regulation of the Synthesis and Release of Slow-reacting Substance of Anaphylaxis From Sensitized Monkey Lung. J Pharmacol Exp Ther. 1982;221(2):295-302. PubMed PMID: 6176708.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of the synthesis and release of slow-reacting substance of anaphylaxis from sensitized monkey lung. AU - Weichman,B M, AU - Hostelley,L S, AU - Bostick,S P, AU - Muccitelli,R M, AU - Krell,R D, AU - Gleason,J G, PY - 1982/5/1/pubmed PY - 1982/5/1/medline PY - 1982/5/1/entrez SP - 295 EP - 302 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 221 IS - 2 N2 - Immunological challenge of sensitized fragmented cynomolgus monkey lung with anti-human IgE (immunoglobulin E) induced the appearance of slow reacting substance of anaphylaxis (SRS-A) in the tissue and evoked the release of SRS-A into the Tyrode's supernatant. The elevation of tissue or residual SRS-A levels was maximal 2 min after anti-IgE challenge and remained at that plateau for at least 60 min. The released SRS-A, first detectable 3 to 5 min after challenge, achieved a plateau by 10 min. Both the released and residual SRS-A were similarly inactivated by soybean lipoxidase and were antagonized by FPL 55712 on the guinea-pig ileum. Isoproterenol, 5, 8, 11, 14-eicosatraynoic acid and SK & F 64398 all inhibited the anti-IgE induced elevation in residual SRS-A and blocked SRS-A release. Indomethacin stimulated both the elevation of residual SRS-A and the amount released. Removal of the Tyrode's supernatant containing 209 +/- 73 U of released SRS-A/g of tissue 20 min after anti-IgE resulted in the release of an additional 239 +/- 69 U/g; residual SRS-A levels remained at the plateau level. Incubation of the Tyrode's supernatant from challenged, but not control, tissue with fresh lung tissue caused a 90 +/- 7% inhibition of SRS-A release from the fresh tissue. Leukotriene D4 at 5 to 50 ng/ml (concentrations relevant to SRS-A release) showed a concentration-dependent inhibition of SRS-A release, but no effect on histamine release. Leukotriene C4 at 5 to 50 ng/mg failed to significantly alter the amount of SRS-A release. However, at 150 ng/ml, significant inhibition was observed which, in part, may have been produced by metabolism to leukotriene D4. These results demonstrate a potential role for LTD in regulating the amount of SRS-A released from monkey lung. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/6176708/Regulation_of_the_synthesis_and_release_of_slow_reacting_substance_of_anaphylaxis_from_sensitized_monkey_lung_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=6176708 DB - PRIME DP - Unbound Medicine ER -