Racial differences influence health-related quality-of-life measurements.

We thank Dr Medford for his interest in our recent article in CHEST (August 2011). 1 Prior studies by our group demonstrated that direct instillation of either Mycoplasma pneumoniae or recombinant M pneumoniae community-acquired respiratory distress syndrome toxin (rCARDS Tx) causes a lymphocytic perivascular response and eventually induces a robust peribronchial infl ammation in both rodents and baboons. 2 More recent studies in our primate model found that rCARDS Tx can initiate a T-helper 2 cell response and “asthma-like” lesions with mixed eosinophilic/lymphocytic infi ltration of airways, mucous metaplasia, and focal mucous plugs (unpublished data). Other groups have shown that allergic airway infl ammation impairs the innate host defenses of the lung and results in reduced clearance of M pneumoniae in animal models of asthma. 3 There are increasing data that both M pneumoniae and CARDS Tx play some role in promoting airway infl ammation that could contribute to the onset and clinical course of asthma. The fact that macrolide antibiotics may be of therapeutic benefi t in some patients with asthma is not surprising because macrolides belong to a family of compounds that possess both immunomodulatory and antimicrobial activity. The proven effi cacy of macrolide antibiotics in other chronic respiratory conditions, such as diffuse pan-bronchiolitis, bronchiectasis, and cystic fi brosis, 4 has led some physicians to use macrolides in patients with diffi cult to control asthma. However, whether macrolides “treat” occult atypical bacterial infections or reduce infl ammatory processes is unclear. Thus, routine use of macrolide antibiotics in the management of chronic stable asthma cannot be recommended because of the lack of available evidence for their effi cacy. Despite these facts, however, there is increasing evidence that some asthmatic patients may be chronically infected or colonized with atypical bacteria and may benefi t from macrolide therapy. However, it remains unclear how to best identify this group of patients, as well as the appropriate dose, frequency, and duration of therapy required to eradicate these organisms. Clearly, more research is needed to better elucidate the role of atypical bacteria in the pathogenesis of asthma and to better defi ne the antiinfl ammatory mechanisms of macrolide antibiotics. Only then will we be able to assess the therapeutic value of macrolides in chronic asthma.