Antigen-Induced Contraction of Human Isolated Lung Preparations Passively Sensitized with Monoclonal IgE: Effects of Indomethacin

Abstract

Human isolated lung preparations were passively sensitized using mouse monoclonal dinitrophenyl (DNP)-specific IgE antibodies. The contractile response to antigen (DNP-bovine serum albumin; DNP-BSA) was approximately 80% of the histamine response (50 µM: 0.20 ± 0.03 g/mm²) in bronchial muscle preparations. In passively sensitized pulmonary vascular and parenchymal preparations, the contraction to antigen was negligible. Indomethacin (1.7 µM; 30 min) did not alter the contractile response to DNP-BSA (5 µg/ml) in bronchial tissues. In passively sensitized bronchial muscle preparations stimulated with DNP-BSA, there was a significant increase (2-fold) in prostanoid production. This production was inhibited by indomethacin. These data suggest that endogenous prostaglandins may not play a role in the regulation of human isolated bronchial muscle contraction to antigen in vitro.

Prostacyclin release and receptor activation: differential control of human pulmonary venous and arterial tone

“…Prostacyclin in human pulmonary vessels 793 Norel et al, 1991). These data together may explain why Walch et al (1999) reported PGE 2 -induced relaxations in human pulmonary veins whereas arteries do not relax.…”

Aging-Shifted Prostaglandin Profile in Endothelium as a Factor in Cardiovascular Disorders

“…In endothelium, PGIS is by far the most abundant PG terminal synthase, with its expression level 5–100-fold higher than the other PG terminal synthases [54, 64, 65, 84]. Accordingly, PGI 2 is the most abundant endothelial eicosanoid, with expression levels 10–100-fold higher than that of the other eicosanoids in humans [107, 108] and in animals [54, 97, 109, 110]. …”

“…PGI 2 triggers potent vasodilation [51, 57] by interacting with the PGI 2 receptor (IP) (Figure 1), which located in smooth muscle cells [108, 111]. The vasodilation effect of PGI 2 has also been shown in pig coronary arteries at low concentrations [58].…”

Anti‐IgE Response in Human Airways: Relative Contribution of Inflammatory Mediators

“…22 However, the increase in contraction observed upon antigen challenge of human airways in vitro was small (approximately 30%) and in other protocols not observed. [1][2][3][4][5][6][7][8][9][10][11][12][13] This slight modulation in human airways is markedly different from that which was reported for guinea-pig tracheal preparations 23 where potentiation of antigen response was considerable (2to 3-fold) subsequent to the Ind treatment. Undem et al 4 have suggested that in human bronchial muscle preparations prostaglandin E,.…”

“…In contrast, other authors have shown inhibitory, or no effects, of Ind on antigenic challenge in human airways. [1][2][3][4][5][6][7][8][9][10][11][12][13] Recently, Bj/Srck and DahMn 14 have reported that potent LT antagonists and/or 5-1ipoxygenase inhibitors decreased the anti-IgE induced contractions. In other studies, such inhibition could be seen only in presence of additional inhibitors or antagonists.…”