Aspirin and Asthma

K. Suresh Babu, MD, DNB; and Sundeep S. Salvi, MD, DNB, PhD, From the Department of Respiratory Cell and Molecular Biology, University of Southampton, Southampton General Hospital, Southampton, UK.

Disclosures

CHEST. 2000;118(5) 

In This Article

Inflammation in AIA

Chronic, persistent inflammation is the hallmark of patients with AIA. [19] Eosinophils are consistently found in blood, nasal, and bronchial secretions as well as in bronchial biopsy specimens of patients afflicted with AIA. [9] Macrophages are present throughout the respiratory tract and are prominent in the bronchial wall and lumen, [20] while T-lymphocyte counts do not differ from those in patients with other types of asthma or in control subjects. [19] The airway expression of IL-5 is also markedly increased in patients with AIA. [21] IL-5 is the key regulator of eosinophil lineage and is involved in eosinophilopoeisis and in eosinophil recruitment, activation, maturation, and survival enhancement. Bronchial biopsy studies also have revealed that eosinophils are the predominant cells containing LTC4 synthase, the essential enzyme in the LT pathway. The increased number of eosinophils and the presence of an increased amount of LTC4 synthase activity may be responsible for the pathophysiology of AIA.

Viral infections are emerging as a common factor of morbidity attributable to asthma exacerbations and might share this feature with AIA, with inflammation being a common denominator. One hypothesis suggested that in response to a virus, long after the initial exposure, specific lymphocytes are produced that are suppressed by PGE2, which is produced by pulmonary alveolar macrophages. Aspirin inhibits PGE2 production, thereby removing the brake. [22] It also was observed that virally infected cells were more prone for drug and drug metabolite-related toxicity. [23] These findings were supported by the finding that acyclovir inhibited analgesic-induced bronchoconstriction in patients with mild to moderate AIA and decreased the urinary levels of LTE4. [24]

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