JL Ellis, WC Hubbard, S Meeker and BJ Undem
Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.

The ability of antigen to contract passively sensitized tissues was examined in human central (5 to 12 mm) and peripheral (0.5 to 2 mm) bronchi. Both central and peripheral bronchi contracted to ragweed antigen E (RW AgE), and these contractions were virtually abolished by a combination of indomethacin, cysteinyl-leukotriene, and histamine antagonists. There were, however, quantitative differences in contractile responses and in mediator release to RW AgE between central and peripheral bronchi. RW AgE was approximately 20-fold more potent in contracting peripheral bronchi compared with central bronchi. On a per weight of tissue basis, RW AgE released six-fold more histamine, 15- to 20-fold more immunoreactive leukotriene D4 (i-LTD4) and two- to 10-fold more prostanoids in the peripheral bronchi compared with central bronchi. Anti-IgE mimicked the effect of RW AgE with respect to inflammatory mediator release and with respect to the magnitude of the contractile response in peripheral and central bronchi. Anti-IgE, however, was more potent in contracting central than peripheral bronchi. Moreover, in peripheral bronchi, contractile responses to anti- IgE were only partially inhibited by a combination of indomethacin, cysteinyl-leukotriene, and histamine antagonists. These results indicate that the qualitative characteristics of antigen-induced mediator release and muscle contraction are similar in central versus peripheral bronchi. However, RW AgE is much more potent in causing smooth muscle constriction, and is capable of releasing a greater quantity of inflammatory mediators in peripheral bronchi/bronchioles than in the more central bronchi.

This article has been cited by other articles:

				Y. Bai, M. Zhang, and M. J. Sanderson Contractility and Ca2+ Signaling of Smooth Muscle Cells in Different Generations of Mouse Airways Am. J. Respir. Cell Mol. Biol., January 1, 2007; 36(1): 122 - 130. [Abstract] [Full Text] [PDF]

				A. Wohlsen, C. Martin, E. Vollmer, D. Branscheid, H. Magnussen, W-M. Becker, U. Lepp, and S. Uhlig The early allergic response in small airways of human precision-cut lung slices Eur. Respir. J., June 1, 2003; 21(6): 1024 - 1032. [Abstract] [Full Text] [PDF]

				P. Berger, D.-W. Perng, H. Thabrew, S. J. Compton, J. A Cairns, A. R. McEuen, R. Marthan, J.-M. Tunon De Lara, and A. F. Walls Tryptase and agonists of PAR-2 induce the proliferation of human airway smooth muscle cells J Appl Physiol, September 1, 2001; 91(3): 1372 - 1379. [Abstract] [Full Text] [PDF]

				A. WOHLSEN, S. UHLIG, and C. MARTIN Immediate Allergic Response in Small Airways Am. J. Respir. Crit. Care Med., May 1, 2001; 163(6): 1462 - 1469. [Abstract] [Full Text]

				E. ROUX, J.-M. HYVELIN, J.-P. SAVINEAU, and R. MARTHAN Human Isolated Airway Contraction . Interaction between Air Pollutants and Passive Sensitization Am. J. Respir. Crit. Care Med., August 1, 1999; 160(2): 439 - 445. [Abstract] [Full Text]

				P. BERGER, A. F. WALLS, R. MARTHAN, and J.M. T.-d. LARA Immunoglobulin E-induced Passive Sensitization of Human Airways . An Immunohistochemical Study Am. J. Respir. Crit. Care Med., February 1, 1997; 157(2): 610 - 616. [Abstract] [Full Text]