A 35-year-old man has a 5-year history of episodic wheezing and coughing. The episodes are more common during the winter months, and he has noticed that they often follow minor respiratory tract infections. In the period between the episodes, he can breathe normally. There is no family history of asthma or other allergies. On physical examination, there are no remarkable findings. A chest radiograph shows no abnormalities. A serum IgE level and WBC count are normal. Which of the following is the most likely mechanism that contributes to the findings in his illness?
This history is typical of nonatopic, or intrinsic, asthma. There is no family history of asthma, no eosinophilia, and a normal serum IgE level. The fundamental abnormality in such cases is bronchial hyperresponsiveness (i.e., the threshold of bronchial spasm is intrinsically low). When airway inflammation occurs after viral infections, the bronchial smooth muscle spasms, and an asthmatic attack occurs. Such bronchial hyperreactivity also may be triggered by inhalation of air pollutants, such as ozone, sulfur dioxide, and nitrogen dioxides. Even exercise and cold air may act as a trigger. Accumulation of neutrophils is typical of bacterial pneumonia, which could follow viral infection, but lead to lung consolidation. Bronchopulmonary aspergillosis refers to colonization of asthmatic airways by Aspergillus, which is followed by development of additional IgE antibodies. Secretion of interleukin (IL)-4 and IL-5 by type 2 helper T cells also occurs in cases of allergic asthma.
Accumulation of alveolar neutrophilic exudate
Bronchial hyperreactivity to chronic inflammation
Emigration of eosinophils into bronchi
Hyperresponsiveness to Aspergillus spores
Respiration