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*
The Joy McCann Culverhouse Airway Disease Research Center, Division of Allergy and Immunology, Department of Internal Medicine, and
Department of Medical Microbiology and Immunology, University of South Florida, and James A. Haley Veterans Affairs Hospital, Tampa, FL 33612; and
Department of Medicine, University of Minnesota, Minneapolis, MN 55415
Respiratory syncytial virus (RSV) infection is considered a risk
factor for bronchial asthma; however, the synergy between allergen
sensitization and RSV infection in the development of pulmonary
inflammation and asthma has been controversial. In this study the
effects of primary and recurrent RSV infection on allergic asthma were
examined in a group of control, RSV-infected, Dermatophagoides
farinae (Df) allergen-sensitized, and
Df allergen-sensitized plus RSV-infected BALB/c mice.
Primary RSV infection in Df-sensitized mice transiently
increases airway responsiveness, which is accompanied by increases in
eosinophilic infiltration, the expression of ICAM-1, and macrophage
inflammatory protein-1
(MIP-1) in the lung tissue. A secondary
RSV infection persistently enhances airway responsiveness in
Df-sensitized mice, with a concomitant increase in
MIP-1 and RSV Ag load in lung tissues. Bulk cultures of thoracic
lymph node mononuclear cells demonstrate that acute RSV infection
augments both Th1- and Th2-like cytokines, whereas secondary and
tertiary infections shift the cytokine profile in favor of the Th2-like
cytokine response in Df-sensitized mice. The elevated
total serum IgE level in the Df-sensitized mice persists
following only RSV reinfection. Thus, recurrent RSV infections in
Df-sensitized mice augment the synthesis of Th2-like
cytokines, total serum IgE Abs, and MIP-1, which are responsible for
persistent airway inflammation and hyperresponsiveness, both of which
are characteristics of asthma.
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