Respiratory syncytial virus protects against the subsequent development of Japanese cedar pollen-induced allergic responses.
Respiratory syncytial virus (RSV) infection has been hypothesized to be a risk factor for the development of allergy and asthma, but epidemiologic studies in humans still remain inconclusive. The association between RSV infection and allergic diseases may be dependent on atopic background and previous history of RSV infection. In this study, the influence of the timing of RSV infection on the development of Japanese cedar pollen (JCP)-induced allergic responses was examined. BALB/c mice were intranasally infected with RSV before or after sensitization to JCP. Production of cytokines in the culture fluid of lung parenchyma cells and the level of antigen-specific antibodies in the serum were determined. It became clear that JCP was a strong inducer for the elicitation of Th2-type responses, characterized by production of interleukin (IL)-4 and IL-5 in the lung and JCP-specific IgE antibody in the serum. RSV infection, however, suppressed JCP-induced allergic responses by decreasing the production of Th2-like cytokines and Th2-type antibodies. This phenomenon was observed more clearly in the groups that were infected with RSV, 2 weeks or 2 days before sensitization to JCP. The inhibitory mechanism of RSV infection seems to be due to RSV-induced Th1 type dominant environment, which down-regulated the Th2-type responses subsequently induced by allergen sensitization. On the other hand, JCP-inoculation altered RSV-induced immune responses to shift from Th1- to Th2-type dominance, by inhibiting RSV-induced Th1-like cytokine production. These data provide evidence that under a certain condition, RSV infection may play a protective role in JCP-induced allergic responses.
Liu
Beixing
B
Department of Microbiology, Fukui University School of Medicine, Fukui, Japan.
Kimura
Yoshinobu
Y
D000485:Allergens / Q000009:adverse effects / Q000276:immunology; D000818:Animals; D000906:Antibodies / Q000097:blood / Q000276:immunology; D000914:Antibodies, Viral / Q000097:blood / Q000276:immunology; D000918:Antibody Specificity; D028203:Cedrus / Q000276:immunology; D015536:Down-Regulation; D007114:Immunization; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007371:Interferon-gamma / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000276:immunology / Q000302:isolation & purification; D015848:Interleukin-5 / Q000276:immunology / Q000302:isolation & purification; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011058:Pollen / Q000009:adverse effects / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000097:blood; D012136:Respiratory Syncytial Viruses / Q000276:immunology*; D006255:Rhinitis, Allergic, Seasonal / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D013997:Time Factors
D000485:Allergens; D000906:Antibodies; D000914:Antibodies, Viral; D015848:Interleukin-5; D018664:Interleukin-12; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma