Open AccessEffect of respiratory syncytial virus on subsequent allergic sensitization to ovalbumin in guinea‐pigs
Author(s) -
Dakhama A.,
Bramley A.m,
Chan N.g,
McKay K.o,
Schellenberg R.r,
Hegele R.g
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.13e08.x
Subject(s) - ovalbumin , medicine , immunology , eosinophilia , sensitization , antibody , bronchiolitis , asthma , respiratory system , pathogenesis , virus , immune system
Children with acute respiratory syncytial virus (RSV) bronchiolitis often develop recurrent wheezing, asthma and allergic sensitization, but the role of RSV in the pathogenesis of these sequelae is unclear. This study examined whether RSV infection potentiates subsequent allergic sensitization, airway hyperresponsiveness (AHR) and airway inflammation induced by repeated exposures to aerosolized ovalbumin (OA) in guinea‐pigs. Guinea‐pigs received either RSV or sham inoculum, followed by exposures to OA‐ or saline‐containing aerosols to form the following groups: 1) noninfected, nonsensitized controls (sham/saline group); 2) RSV‐infected, nonsensitized animals (RSV/saline group); 3) noninfected, OA‐sensitized animals (sham/OA group); 4) RSV infection and first OA exposure on the same day (RSV/OA group), and 5) RSV infection six days prior to first OA exposure (RSV6/OA group). Three days after the final aerosol exposure, circulating OA‐specific immunoglobulin (Ig)G 1 antibody titres and AHR to inhalation acetylcholine challenge were measured and morphometry performed to evaluate allergic inflammation of the airways. OA‐exposed animals developed OA‐specific IgG 1 antibodies, AHR and airway eosinophilia (sham/OA, RSV/OA and RSV6/OA groups. RSV infection alone induced significant AHR and airway eosinophilia (RSV/saline group). RSV infection, and concomitant exposure to OA (RSV/OA group) enhanced OA‐specific IgG 1 antibodies, but not airway eosinophilia or AHR. Such increases were not observed in the RSV6/OA group. In conclusion, respiratory syncytial virus potentiates the production of ovalbumin‐specific immunoglobulin G 1 antibodies in guinea‐pigs, but circulating titres of these antibodies do not reflect the extent of airway hyperresponsiveness or airway inflammation. In addition, respiratory syncytial virus infection alone can produce slight increases in airway hyperresponsiveness that are associated with increased numbers of eosinophils in the airways.