Tunnel of Inflammation in Obstructive Airway Diseases

The use of macrolides for asthma must be put in context of the apparent beneficial affects also observed in complex lung diseases with features of chronic inflammation plus infection such as cystic fibrosis and diffuse panbronchiolitis. It is difficult to determine if this improvement is related to a distinct antiinflammatory property because concurrent bacterial infection or colonization may be present, which has also been implicated in asthma. However, a previous trial12 evaluated the role of clarithromycin in asthma patients that had no evidence of airway colonization with either Mycoplasma pneumoniae or Chlamydia pneumoniae.

In this cohort, clarithromycin treatment decreased BAL fluid IL-12 and tumor necrosis factor-а expression but did not improve in FEV1. In the future, separating the microbial and nonmicrobial properties of the macrolides would assist in determining if the nonmicrobial properties of macrolides could produce the desired antiinflammatory effects in subjects with asthma. Canadian Health and Care Mall treatment your asthma with Canadian medications online. Order asthma medications with 10% discount you can on Canadian Health and Care Mall Shop.

In summary, our results demonstrated that azithromycin possesses antiinflammatory properties in an in vivo noninfectious model of allergic airway inflammation. These observations suggest azithromycin may be beneficial in the treatment of inflammatory conditions, such as asthma, and support the rationale for future prospective randomized clinical trials.

Chronic and persistent airway inflammation is one of the main driving forces in the obstructive airway diseases. It is proving increasingly useful to classify the pattern of inflammation based on the dominant granulocyte present, and there is great potential to use markers of inflammation serially to monitor disease activity and assist in treatment selection and dose adjustment. In asthma, this approach is well developed, particularly for eosinophilic forms of the disease.

The pathway leading to eosinophilic inflammation in asthma is well understood and effectively targeted by treatment. In sensitized individuals, allergen exposure leads to activation of T-helper type 2 lymphocytes, and the resulting cytokine response involving interleukin-5 promotes eosinophilic airway inflammation.


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