[The role of infection in asthma]

Since the first decades of the twentieth century, some authors have believed bacterial respiratory infection to be an important triggering factor in bronchial asthma, drawing attention to an asthmatic response to infection. In this context, already in 1995, we presented a study on nasal secretion cultures and the relationship between IgE and sensitization to allergens. There was a statistically significant association between patients with sensitization to Dermatophagoides, elevated IgE levels and Staphylococcus Aureus positive cultures. Following the studies by Norn, we performed a study in 40 children, aged 2-14 years, and observed that these children with sensitization to mites and positive culture released higher histamine levels than did children with negative cultures and controls. The differences were statistically significant. In agreement with other authors, we also found that the presence of both S. aureus and D. pteronyssinus favored antigen specific histamine release. In the last few years, when the increase in the prevalence of bronchial asthma began to be studied, the role of infection, among other factors, in favoring this increase began to be examined. Using the methodology of the ISAAC project, we distributed a parallel questionnaire containing questions on triggering and contributing factors among which was respiratory infection. We found that there was an association between having three of more episodes of bronchitis in the previous year, accompanied by fever and with a duration of more than 7 days and having asthma at some time (OR: 29.09). This association was even higher in patients with wheezing in the previous 12 months (OR: 43.26) and was also associated with the need to present to the emergency department (OR: 30.65). From these results we conclude that respiratory infection is an aggravating factor in asthma, as we already know. For several years, several authors have studied how non-nosocomial respiratory infections can directly modulate Th1/Th2 response. In order to obtain our own results, we studied serum interleukin 4 (IL4) and interferon-gamma (IFN-gamma) in 42 children aged 3-17 years. The most frequent IL-4 values expressed in ng/ml were between 0.25-0.40, with little variation in the sample, which did not permit correlation among variables. Concerning IFN-gamma, we found values between < 5 and 605 pg/ml. In children undergoing antigen-specific immunotherapy, we observed mean IFN-gamma values of 115.86 pg/ml, while children not undergoing immunotherapy and those who had been administered this treatment for less than 1 year, had a mean of 66.06 pg/ml. These differences were statistically significant (p = 0.035), thus revealing a Th1 response to immunotherapy. These differences were not statistically significant when children who had been administered immunotherapy for less than 1 year were included. When we studied children with bacterial immunotherapy and grouped them in the same way, we found that the mean IFN-gamma of the children undergoing immunotherapy for more than 1 year was 56.4 pg/ml compared with 101.75 pg/ml in those without immunotherapy. This difference was statistically significant (p = 0.034). We are able to conclude that bacterial immunotherapy modifies Th1 response, inhibiting it in children with higher susceptibility to infection. In view of these preliminary results, it would be interesting to continue to study interleukins in order to determine the modification of these substances by immunotherapy in a prospective study and with a sample selected in relation to immunotherapy and not other parameters, since those we have studied have shown no relationship.