Modulation of systemic and mucosal immune responses to inhaled ragweed antigen in experimentally induced infection with respiratory syncytial virus implication in virally induced allergy.
Groups of BALB/c mice were either sham-infected or infected intranasally with respiratory syncytial virus (RSV). On the third day following intranasal inoculation, all groups of mice were exposed by inhalation to ragweed antigen for 5 consecutive days and rechallenged with ragweed on day 31. Development of antibody activity to ragweed antigen was examined in serum and bronchial washings at regular intervals employing an ELISA assay for IgG and IgA antibody activity and passive cutaneous anaphylaxis for IgE-specific responses. The serum IgG and IgE antibody response to ragweed following primary exposure developed at significantly higher levels in mice previously infected with RSV, compared to sham-infected controls. In addition, an earlier rise in serum IgE response to ragweed occurred in the RSV-infected animals. IgG and IgA anti-ragweed antibody activity in bronchial washings was also observed with significantly higher levels in the RSV-infected animals when compared to the controls, although a similar increase in antigen-specific IgE activity in bronchial washings was found in both groups of animals. These findings support the possibility that mucosally restricted virus infections of the respiratory tract may enhance the development of sensitization and the magnitude of antibody responses to other inhaled allergens found concomitantly in the respiratory tract during acute infection.
Leibovitz
E
E
Department of Pediatrics, State University of New York, Buffalo.
Freihorst
J
J
Piedra
P A
PA
Ogra
P L
PL
D000280:Administration, Inhalation; D000818:Animals; D000917:Antibody Formation; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D005260:Female; D006967:Hypersensitivity / Q000382:microbiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D011058:Pollen / Q000276:immunology*; D012136:Respiratory Syncytial Viruses; D010253:Respirovirus Infections / Q000276:immunology* / Q000503:physiopathology; D014779:Virus Replication