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Jay I. Peters, MD, FCCP; Edward G. Brooks, MD; Harjinder Singh, MD
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From the Department of Medicine (Drs Peters and Singh) and Pediatrics (Dr Brooks), University of Texas Health Science Center at San Antonio.

Correspondence to: Jay I. Peters, MD, FCCP, Department of Medicine, University of Texas Health Science Center at San Antonio, 7704 Floyd Curl Dr, San Antonio, TX 78229; e-mail: Peters@uthscsa.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(2):570. doi:10.1378/chest.11-2909
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To the Editor:

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 inflammation 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lesions with mixed eosinophilic/lymphocytic infiltration of airways, mucous metaplasia, and focal mucous plugs (unpublished data). Other groups have shown that allergic airway inflammation 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 inflammation that could contribute to the onset and clinical course of asthma.

The fact that macrolide antibiotics may be of therapeutic benefit 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 efficacy of macrolide antibiotics in other chronic respiratory conditions, such as diffuse pan-bronchiolitis, bronchiectasis, and cystic fibrosis,4 has led some physicians to use macrolides in patients with difficult to control asthma. However, whether macrolides “treat” occult atypical bacterial infections or reduce inflammatory 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 efficacy. Despite these facts, however, there is increasing evidence that some asthmatic patients may be chronically infected or colonized with atypical bacteria and may benefit 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 define the antiinflammatory mechanisms of macrolide antibiotics. Only then will we be able to assess the therapeutic value of macrolides in chronic asthma.

Peters J, Singh H, Brooks EG, et al. Persistence of community-acquired respiratory distress syndrome toxin-producingMycoplasma pneumoniaein refractory asthma. Chest. 2011;1402:401-407 [PubMed] [CrossRef]
 
Hardy RD, Coalson JJ, Peters J, et al. Analysis of pulmonary inflammation and function in the mouse and baboon after exposure to Mycoplasma pneumoniae CARDS toxin. PLoS ONE. 2009;410:e7562 [PubMed]
 
Wu Q, Martin RJ, Lafasto S, et al. Toll-like receptor 2 down-regulation in established mouse allergic lungs contributes to decreased mycoplasma clearance. Am J Respir Crit Care Med. 2008;1777:720-729 [PubMed]
 
Friedlander AL, Albert RK. Chronic macrolide therapy in inflammatory airways diseases. Chest. 2010;1385:1202-1212 [PubMed]
 

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References

Peters J, Singh H, Brooks EG, et al. Persistence of community-acquired respiratory distress syndrome toxin-producingMycoplasma pneumoniaein refractory asthma. Chest. 2011;1402:401-407 [PubMed] [CrossRef]
 
Hardy RD, Coalson JJ, Peters J, et al. Analysis of pulmonary inflammation and function in the mouse and baboon after exposure to Mycoplasma pneumoniae CARDS toxin. PLoS ONE. 2009;410:e7562 [PubMed]
 
Wu Q, Martin RJ, Lafasto S, et al. Toll-like receptor 2 down-regulation in established mouse allergic lungs contributes to decreased mycoplasma clearance. Am J Respir Crit Care Med. 2008;1777:720-729 [PubMed]
 
Friedlander AL, Albert RK. Chronic macrolide therapy in inflammatory airways diseases. Chest. 2010;1385:1202-1212 [PubMed]
 
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