Immunologic and Physiologic Characterization of the Role of Reaginic Antibodies in Experimental Asthma in Dogs

Kessler, G; Frick, Oscar L.; Gold, Warren M.

doi:10.1159/000231225

Cited by 29 publications

(8 citation statements)

References 11 publications

(13 reference statements)

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“…The heat-labile nature of the serum suggests that the sensitizing component was a reaginic antibody of the immunoglobulin E type. This observation is consistent with those of others who have demonstrated that antibodies mediating canine immedi ate hypersensitivity type reactions in vivo closely resemble human reagin ic antibody of the IgE type [Patterson and Sparks, 1962;Patterson et al, 1963;Kessler et al, 1974], The significant but weak correlation between histamine and SRS-A re lease by antigen challenge in actively and passively sensitized lung con notes the possibility of an interrelationship between these two substances. These results are at variance with those obtained in fragmented human lung where no correlation could be established [Orange and Langer, 1974], However, the possibility of a relationship between these mediators in canine lung may be more apparent than real as passive sensitization appeared to favor the enhancement of histamine release compared to SRS-A.…”

Section: Discussionsupporting

confidence: 91%

An <i>in vitro</i> Model of Canine Immediate-Type Hypersensitivity Reactions

Krell¹,

Chakrin²

1976

Int Arch Allergy Immunol

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Fragmented lung prepared from dogs cutaneously sensitive to ascaris antigen released histamine and a slow-reacting substance of anaphylaxis-like (SRS-A) material upon antigen challenge. Passive sensitization of fragments with serum obtained from ascaris-sensitive donor dogs enhanced the release of both substances; heating (56 °C for 4 h) destroyed the ability of the serum to enhance release. In passively sensitized tissues isoproterenol and papaverine inhibited the release of histamine and SRS-A; propranolol antagonized the effect of isoproterenol. Carbachol enhanced the release of both substances from passively sensitized lung whereas disodium cromoglycate and aminoguanidine were without effect. It is concluded that fragmented canine lung is a useful model for study of immediate-type hypersensitivity reactions.

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Section: Discussionsupporting

confidence: 91%

An <i>in vitro</i> Model of Canine Immediate-Type Hypersensitivity Reactions

Krell¹,

Chakrin²

1976

Int Arch Allergy Immunol

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“…These changes in pulmonary mechanics resemble, in many respects, those documented clinically in allergic asthmatic patients undergoing an acute episode (Yu, Gallant & Gold, 1972;Rosenthal, Norman & Summer, 1975). Furthermore, this response to ascaris antigen appears to be mediated by a reaginic antibody (Kessler, Frick & Gold, 1974) which possesses physicochemical and biological characteristics similar to human reaginic antibody of the immunoglobulin E class (Patterson & Sparks, 1962; Patterson, Pruzansky & Chang, 1963; Schwartzman, Rockey & Halliwell, 1971;Kessler et al, 1974).…”

Section: Introductionsupporting

confidence: 55%

Investigation of the Role of Histamine in Antigen‐induced Bronchoconstriction in the Ascaris‐hypersensitive Dog

Krell¹

1978

British J Pharmacology

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1 Aerosol administration of ascaris antigen to the airways of ascaris-hypersensitive dogs provoked increases in pulmonary resistance (Rp) and decreases in dynamic lung compliance (Cdyn). These changes in pulmonary mechanics were not inhibited by the histamine H1-receptor antagonists, diphenhydramine or mepyramine. 2 Increases in Rp and decreases in Cdyn induced by a histamine aerosol were markedly or totally inhibited by comparable doses of these HI-antihistamines.3 Doses of antigen which produced pathophysiological pulmonary responses failed to produce a detectable histamine release from the cardiopulmonary system in vitio. Aerosol antigen provocation, equivalent to 5 to 9 times greater than that which produced substantial pathophysiological pulmonary responses, did cause histamine release in vivo. 4 The canine cardiopulmonary system showed only a modest ability to remove and/or degrade circulating histamine. 5 It is concluded that histamine may not play a major role in mediating the acute antigen-induced bronchoconstriction in the ascaris-hypersensitive dog.

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“…Experimental bronchial asthma produced by ascaris suum was found to result from reaginic antibodies in dogs (17) and in monkeys (9,18). Inhalation of cromolyn prominently inhibits the increase in respiratory resistance produced by exposure of Asc-Ag aerosol (16).…”

Section: Discussionmentioning

confidence: 99%

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

Yamatake

Sasagawa

Yanaura

et al. 1977

Japanese Journal of Pharmacology

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Abstract-Participationof histamine H1 and H2-receptors in both asthmas, i.e. experimentally induced bronchoconstriction and bronchosecretion, with ascaris suum and histamine in anesthetized dogs was investigated.Dogs given 0.2% histamine solution or ascaris antigen (3 mg protein) by inhalation showed increases in respiratory resistance (Rrs) and respiratory rate to 2.5-5.0 fold. Airway secretion volume was also significantly increased 3-4 fold. The increase in Rrs by histamine inhalation was effectively inhibited or abolished by a histamine HI-receptor antagonist, chlorphenira mine (0.3-1 mg/kg i.v.), but not by a H2-receptor antagonist, cimetidine (1-3 mg/kg i.v.). The increase in Rrs by antigen inhalation was reduced by relatively high doses of chlorpheniramine (1-3 mg/kg i.v.), and not by cimetidine.In contrast, hyperse cretion of tracheobronchial fluid in both asthmas was significantly prevented by either chlorpheniramine or cimetidine. Combinations of both antagonists abolished the hypersecretion.Atropine (2 mg/kg i.v.) significantly inhibited the occurrence of responses in both asthmas. The results suggest that histamine is involved in the allergic asthma produced by ascaris suum and that histamine directly evokes airway constriction through Hl-receptors and hypersecretion of tracheobronchial fluid through H1 and H2-receptors, and, in a part, indirectly activates the cholinergic pathway.There has been much evidence that histamine is the chief chemical mediator released from mast cells during anaphylaxis (1-9).Experimental bronchial asthma in guinea pigs is prominently inhibited by classical antihistamines (10-12). Schild et al. (3) showed un equivocally that histamine release occurs in bronchial tissue of an asthmatic patient.Ash and Schild (13) demonstrated two types of histamine receptors and Black et al.(14) introduced specific antagonists of these receptors which made it possible to characterize and locate these receptors in the body. Data of the presence of H1 and H2-receptors in airway smooth muscle in different species have been documented, and are cited in the review of Chand and Eyre (15). There are, however, specifically no reports on the distribution of these receptors in the dog airway smooth muscle or on the role of these receptors in bron chosecretion. We attempted to characterize histamine receptors responsible for airway constriction and hypersecretion which occurs in ascaris and histamine-induced asthmas, using histamine H1 and H2-receptor antagonists. MATERIALS AND METHODSMale mongrel dogs weighing between 6 and 17 kg were anesthetized with sodium

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Immunologic and Physiologic Characterization of the Role of Reaginic Antibodies in Experimental Asthma in Dogs

Cited by 29 publications

References 11 publications

An <i>in vitro</i> Model of Canine Immediate-Type Hypersensitivity Reactions

An <i>in vitro</i> Model of Canine Immediate-Type Hypersensitivity Reactions

Investigation of the Role of Histamine in Antigen‐induced Bronchoconstriction in the Ascaris‐hypersensitive Dog

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

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