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.