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Richard F. Lockey, MD; Samuel C. Bukantz, MD

JAMA. 1986;256(15):2076-2077.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Among the most significant contributions to the treatment of the asthmatic patient is the recognition that a second or delayed response by the allergic asthmatic patient to antigen exposure, termed late phase reaction (LPR), is an inflammatory reaction. The LPR has been observed in the skin, the lung, and the nose.

The neutrophil leukocyte is the dominant cell in these reactions, although mononuclear cells, basophils, and eosinophils participate. There is evidence that soluble factors (histamine-releasing activity from neutrophils) stimulate redegranulation of mast cells that contributes to the induction of bronchial hyperreactivity.¹ This inflammatory component is also induced by irritants, such as cold air and ozone, and infectious agents, such as viruses. This has permitted rational interpretation of previously poorly understood clinical and experimental observations. It has stimulated more research and aggressive therapy for both allergic and nonallergic types of asthma with cromolyn (a mast cell—stabilizing agent), oral cromolynlike drugs . . . [Full Text PDF of this Article]

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