Respiratory infection in asthma.
Ever since the first decades of the 20th century, some authors have given respiratory infection triggered by bacteria an etiologic role in bronchial asthma, focusing on infection and the asthmatic response. In 1995 our group already presented a study in this sense on nasal secretion cultures and the relationship between IgE and sensitization to allergens. There is a significant association between patients with sensitization to Dermatophagoides, high levels of total IgE, and positive culture to Staphylococcus aureus. Following studies by Norn, we performed a study with 40 children, aged 2-14 years, where we observed that children with sensitization to mites and a positive culture had higher levels of histamine release than did children with negative culture and controls, the differences being significant. We also found, like other authors, that the joint presence of Staphylococcus aureus and Derrmatophagoides pteronyssinus potentiates antigen-specific histamine release. In recent years, with the increasing prevalence of bronchial asthma being studied, the role that infection could play in this increase is being considered again among other factors. As participants of the ISAAC project and using the same methods as in this study, we performed a simultaneous questionnaire with questions related with triggering and contributing factors, etc., including respiratory infection. We found an association between having had more than three episodes of "bronchitis" with fever and lasting for longer than seven days in the last year and having ever had asthma (OR 29.09). This association is still greater with having had wheezing in the last 12 months (OR 43.26), a finding that it is also associated with requiring attention in an emergency room (OR 30.65). From these results, we concluded that respiratory infection is an aggravating factor of asthma, something we already knew. In order to have our own experience, we studied serum interleukin 4 (IL-4) and interferon gamma (IFNgamma) in a sample of 41 children aged 3 to 17 years. The most frequent values of IL-4 ranged between 0.25 and 0.40 ng, and very low dispersion was found in the sample, which did not allow correlation with other parameters. Regarding IFNgamma, we found values between < 5 pg/ml and 605 pg/ml. When we studied children under treatment with antigen-specific immunotherapy, we observed mean values of IFNgamma of 115.86 pg/ml, whereas the ones who did not follow this treatment or had followed it for less than one year had a mean of 66.06 pg/ml, these differences being significant (p = 0.035), and proving a Th1 response to immunotherapy. This significance is not found if children who have been under immunotherapy for less than one year are included. When we studied children with bacterial immunotherapy, we found that the mean IFNgamma value in children under immunotherapy for longer than one year was 56.4 pg/ml, whereas in children with no immunotherapy it was 101.75 pg/ml (p = 0.034). We conclude that bacterial immunotherapy modifies the Thl response, inhibiting it in those children with greater susceptibility to infections.