TY - JOUR
T1 - Recurrent respiratory syncytial virus infections in allergen-sensitized mice lead to persistent airway inflammation and hyperresponsiveness
AU - Matsuse, Hiroto
AU - Behera, Aruna K.
AU - Kumar, Mukesh
AU - Rabb, Hamid
AU - Lockey, Richard F.
AU - Mohapatra, Shyam S.
PY - 2000/6/15
Y1 - 2000/6/15
N2 - 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-1α (MIP-1α) in the lung tissue. A secondary RSV infection persistently enhances airway responsiveness in Df- sensitized mice, with a concomitant increase in MIP-1α 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- 1α, which are responsible for persistent airway inflammation and hyperresponsiveness, both of which are characteristics of asthma.
AB - 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-1α (MIP-1α) in the lung tissue. A secondary RSV infection persistently enhances airway responsiveness in Df- sensitized mice, with a concomitant increase in MIP-1α 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- 1α, which are responsible for persistent airway inflammation and hyperresponsiveness, both of which are characteristics of asthma.
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U2 - 10.4049/jimmunol.164.12.6583
DO - 10.4049/jimmunol.164.12.6583
M3 - Article
C2 - 10843718
AN - SCOPUS:0034659961
VL - 164
SP - 6583
EP - 6592
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 12
ER -