| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
*
Department of Pharmacology,
Laboratory of Biodynamics, and
Second Department of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan;
Choju Medical Institute, Fukushimura Hospital, Toyohashi, Japan; and
¶ Department of Molecular Biology, Nagoya City University School of Medicine, Nagoya, Japan
We attempted to elucidate the contribution of complement to allergic asthma. Rat sensitized to OVA received repeated intratracheal exposures to OVA for up to 3 consecutive days, and pulmonary resistance was then estimated for up to 6 h after the last exposure. Whereas the immediate airway response (IAR) in terms of RL tended to decrease in proportion to the number of OVA exposures, late airway response (LAR) became prominent only after three. Although premedication with two kinds of complement inhibitors, soluble complement receptor type 1 (sCR1) or nafamostat mesylate, resulted in inhibition of the IAR after either a single or a double exposure, the LAR was inhibited after the triple. Premedication with a C5a receptor antagonist (C5aRA) before every exposure to OVA also inhibited the LAR after three. Repeated OVA exposure resulted in eosinophil and neutrophil infiltration into the bronchial submucosa which was suppressed by premedication with sCR1 or C5aRA. Up-regulation of C5aR mRNA was shown in lungs after triple OVA exposure, but almost no up-regulation of C3aR. Pretreatment with sCR1 or C5aRA suppressed the up-regulation of C5aR expression as well as cytokine messages in the lungs. The suppression of LAR by pretreatment with sCR1 was reversed by intratracheal instillation of rat C5a desArg the action of which was inhibited by C5aRA. In contrast, rat C3a desArg or cytokine-induced neutrophil chemoattractant-1 induced cellular infiltration into the bronchial submucosa by costimulation with OVA, but these had no influence on the LAR. These differences might be explained by the fact that costimulation with OVA and C5a synergistically potentiated IAR, whereas that with OVA and either C3a or cytokine-induced neutrophil chemoattractant-1 did not. C5a generated by Ag-Ab complexes helps in the production of cytokines and contributes to the LAR after repeated exposure to Ag.
This article has been cited by other articles:
|
|
 |
|
  M. Wills-Karp Complement Activation Pathways: A Bridge between Innate and Adaptive Immune Responses in Asthma Proceedings of the ATS, July 1, 2007; 4(3): 247 - 251. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Taube, J. M. Thurman, K. Takeda, A. Joetham, N. Miyahara, M. C. Carroll, A. Dakhama, P. C. Giclas, V. M. Holers, and E. W. Gelfand Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammation PNAS, May 23, 2006; 103(21): 8084 - 8089. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Drouin, M. Sinha, G. Sfyroera, J. D. Lambris, and R. A. Wetsel A Protective Role for the Fifth Complement Component (C5) in Allergic Airway Disease Am. J. Respir. Crit. Care Med., April 15, 2006; 173(8): 852 - 857. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Murai, M. Abe, Y. Hayashi, N. Sakata, T. Katsuragi, and K. Tanaka Comparison Study between the Mechanisms of Allergic Asthma Amelioration by a Cysteinyl-Leukotriene Type 1 Receptor Antagonist Montelukast and Methylprednisolone J. Pharmacol. Exp. Ther., February 1, 2005; 312(2): 432 - 440. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Baelder, B. Fuchs, W. Bautsch, J. Zwirner, J. Kohl, H. G Hoymann, T. Glaab, V. Erpenbeck, N. Krug, and A. Braun Pharmacological Targeting of Anaphylatoxin Receptors during the Effector Phase of Allergic Asthma Suppresses Airway Hyperresponsiveness and Airway Inflammation J. Immunol., January 15, 2005; 174(2): 783 - 789. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Marc, P. Korosec, M. Kosnik, I. Kern, M. Flezar, S. Suskovic, and J. Sorli Complement Factors C3a, C4a, and C5a in Chronic Obstructive Pulmonary Disease and Asthma Am. J. Respir. Cell Mol. Biol., August 1, 2004; 31(2): 216 - 219. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Hogaboam, K. Takahashi, R. A. B. Ezekowitz, S. L. Kunkel, and J. M. Schuh Mannose-binding lectin deficiency alters the development of fungal asthma: effects on airway response, inflammation, and cytokine profile J. Leukoc. Biol., May 1, 2004; 75(5): 805 - 814. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-W. Park, C. Taube, A. Joetham, K. Takeda, T. Kodama, A. Dakhama, G. McConville, C. B. Allen, G. Sfyroera, L. D. Shultz, et al. Complement Activation Is Critical to Airway Hyperresponsiveness after Acute Ozone Exposure Am. J. Respir. Crit. Care Med., March 15, 2004; 169(6): 726 - 732. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Taube, Y.-H. Rha, K. Takeda, J.-W. Park, A. Joetham, A. Balhorn, A. Dakhama, P. C. Giclas, V. M. Holers, and E. W. Gelfand Inhibition of Complement Activation Decreases Airway Inflammation and Hyperresponsiveness Am. J. Respir. Crit. Care Med., December 1, 2003; 168(11): 1333 - 1341. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Drouin, D. B. Corry, T. J. Hollman, J. Kildsgaard, and R. A. Wetsel Absence of the Complement Anaphylatoxin C3a Receptor Suppresses Th2 Effector Functions in a Murine Model of Pulmonary Allergy J. Immunol., November 15, 2002; 169(10): 5926 - 5933. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
