| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Division of Respiratory Diseases and Allergy, Centre for Gene Therapeutics and Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada; and
Department of Medicine, University of Vermont, Burlington, VT 05405
Corticosteroids (CS) remain the most efficacious pharmacotherapeutic option for the management of asthma. Although the acute anti-inflammatory effects of CS treatment have been amply documented both clinically and experimentally, recent human data intimate that exposure to CS may be associated with retrograde immune phenomena, including enhanced synthesis of IgE in vivo and elevated Th2 cytokine production in vitro. We have investigated the long-term immunologic effects of CS treatment in a murine model of allergic airway inflammation. CS treatment during initial exposure to OVA or upon long-term Ag rechallenge remarkably attenuated eosinophilic airway inflammation and airway hyperresponsiveness. Interestingly, however, Th2 cytokine production by cultured splenocytes from CS-treated mice was significantly elevated, while IFN-
synthesis was depressed. Moreover, mice rechallenged with OVA several weeks after CS intervention during allergic sensitization not only developed airway inflammation, but also exhibited enhanced Th2 cytokine production in lymphoid tissues and OVA-specific IgE in serum. This amplification of the systemic immune response was associated with an intact APC compartment during CS-conditioned sensitization to OVA. These data indicate that immune processes underlying the allergic phenotype remain impervious to CS treatment and raise the possibility that treatment with CS during sensitization may amplify elements of the allergen-specific immune response.
This article has been cited by other articles:
|
|
 |
|
  D. S. Southam, R. Ellis, J. Wattie, W. Glass, and M. D. Inman Goblet Cell Rebound and Airway Dysfunction with Corticosteroid Withdrawal in a Mouse Model of Asthma Am. J. Respir. Crit. Care Med., December 1, 2008; 178(11): 1115 - 1122. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Johnson, S. R. Pacitto, J. Wong, E. W. Archer, S. Eirefelt, A. Miller-Larsson, and M. Jordana Combined budesonide/formoterol therapy in conjunction with allergen avoidance ameliorates house dust mite-induced airway remodeling and dysfunction Am J Physiol Lung Cell Mol Physiol, November 1, 2008; 295(5): L780 - L788. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Nagamachi, D. Sakata, K. Kabashima, T. Furuyashiki, T. Murata, E. Segi-Nishida, K. Soontrapa, T. Matsuoka, Y. Miyachi, and S. Narumiya Facilitation of Th1-mediated immune response by prostaglandin E receptor EP1 J. Exp. Med., November 26, 2007; 204(12): 2865 - 2874. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Stock, O. Akbari, R. H. DeKruyff, and D. T. Umetsu Respiratory Tolerance Is Inhibited by the Administration of Corticosteroids J. Immunol., December 1, 2005; 175(11): 7380 - 7387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. L. Guo, W. Auttachoat, and R. P. Chi Genistein Enhancement of Respiratory Allergen Trimellitic Anhydride-induced IgE Production by Adult B6C3F1 Mice Following In Utero and Postnatal Exposure Toxicol. Sci., October 1, 2005; 87(2): 399 - 408. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
