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Immunopharmacology of anaphylatoxin-induced bronchoconstrictor responses.
Complement. 1986; 3(3):137-51.C

Abstract

The complement anaphylatoxin peptides, C3a and C5a, are potential mediators of immediate hypersensitivity reactions, eliciting many of the same actions on isolated tissue and cell preparations as specific antigen. Instilled intratracheally in experimental animals, the peptides induce acute bronchospasms and are sometimes lethal. In vitro, they cause dose-dependent contraction of isolated lung tissue preparations, a response which correlates well with bronchospasms observed in vivo, and our current understanding of the cellular and molecular mechanisms of this action are reviewed here. C5a and its catabolic derivative, C5ades Arg, stimulate contraction of isolated guinea pig lung parenchymal strips in part by production of leukotrienes that constitute SRS-A, and by release of histamine. Leukotrienes in turn release thromboxane from lung tissue, and evidence indicates that at least part of the spasmogenic activity of these peptidolipids is mediated by this effect. C3a is considerably less potent than C5a in contracting lung tissues and appears to act primarily by causing the release of spasmogenic cyclooxygenase metabolites. Both peptides may additionally have direct action on contractile cells within the tissue. Platelet-activating factor (PAF), an unusual phospholipid mediator released from inflammatory cells stimulated with C5a and other agents, also contracts isolated lung parenchymal tissues. PAF stimulates release of significant quantities of thromboxane from guinea pig lung; however, indomethacin does not block contractile responses of the tissue. Recent evidence indicates that PAF may act on parasympathetic neurons in lung to release endogenous acetylcholine, and this action may be a major component of tissue responses to this mediator. Thus the complement anaphylatoxins stimulate release of many of the same mediators from lung tissues as are released by antigen challenge of sensitized tissue, and may, therefore, play an important role in the pathogenesis of allergic bronchospasms.

Authors

Stimler-Gerard NP
No affiliation info available

MeSH

AnaphylatoxinsAnimalsBronchiBronchial SpasmComplement ActivationComplement C3Complement C3aComplement C5Complement C5aDose-Response Relationship, DrugInflammationLeukotriene B4LungMiceMuscle ContractionPeptidesPlatelet Activating FactorSRS-A

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

3026723

Citation

Stimler-Gerard, N P.. "Immunopharmacology of Anaphylatoxin-induced Bronchoconstrictor Responses." Complement (Basel, Switzerland), vol. 3, no. 3, 1986, pp. 137-51.
Stimler-Gerard NP. Immunopharmacology of anaphylatoxin-induced bronchoconstrictor responses. Complement. 1986;3(3):137-51.
Stimler-Gerard, N. P. (1986). Immunopharmacology of anaphylatoxin-induced bronchoconstrictor responses. Complement (Basel, Switzerland), 3(3), 137-51.
Stimler-Gerard NP. Immunopharmacology of Anaphylatoxin-induced Bronchoconstrictor Responses. Complement. 1986;3(3):137-51. PubMed PMID: 3026723.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunopharmacology of anaphylatoxin-induced bronchoconstrictor responses. A1 - Stimler-Gerard,N P, PY - 1986/1/1/pubmed PY - 1986/1/1/medline PY - 1986/1/1/entrez SP - 137 EP - 51 JF - Complement (Basel, Switzerland) JO - Complement VL - 3 IS - 3 N2 - The complement anaphylatoxin peptides, C3a and C5a, are potential mediators of immediate hypersensitivity reactions, eliciting many of the same actions on isolated tissue and cell preparations as specific antigen. Instilled intratracheally in experimental animals, the peptides induce acute bronchospasms and are sometimes lethal. In vitro, they cause dose-dependent contraction of isolated lung tissue preparations, a response which correlates well with bronchospasms observed in vivo, and our current understanding of the cellular and molecular mechanisms of this action are reviewed here. C5a and its catabolic derivative, C5ades Arg, stimulate contraction of isolated guinea pig lung parenchymal strips in part by production of leukotrienes that constitute SRS-A, and by release of histamine. Leukotrienes in turn release thromboxane from lung tissue, and evidence indicates that at least part of the spasmogenic activity of these peptidolipids is mediated by this effect. C3a is considerably less potent than C5a in contracting lung tissues and appears to act primarily by causing the release of spasmogenic cyclooxygenase metabolites. Both peptides may additionally have direct action on contractile cells within the tissue. Platelet-activating factor (PAF), an unusual phospholipid mediator released from inflammatory cells stimulated with C5a and other agents, also contracts isolated lung parenchymal tissues. PAF stimulates release of significant quantities of thromboxane from guinea pig lung; however, indomethacin does not block contractile responses of the tissue. Recent evidence indicates that PAF may act on parasympathetic neurons in lung to release endogenous acetylcholine, and this action may be a major component of tissue responses to this mediator. Thus the complement anaphylatoxins stimulate release of many of the same mediators from lung tissues as are released by antigen challenge of sensitized tissue, and may, therefore, play an important role in the pathogenesis of allergic bronchospasms. SN - 0253-5076 UR - https://www.unboundmedicine.com/medline/citation/3026723/Immunopharmacology_of_anaphylatoxin_induced_bronchoconstrictor_responses_ DB - PRIME DP - Unbound Medicine ER -