Studies on the allergic and nonallergic nasal inflammation

Nasal lavage after antigenic and nonantigenic nasal stimulation has become an important tool for the study of inflammatory phenomena in the upper airway. Biochemical and cytologic information is relatively easily obtainable, and pharmacologic manipulations can be readily monitored. This article is of several studies aiming toward a more profound understanding of the mechanisms of allergic and nonallergic rhinitis by the use of laboratory-challenge procedures and nasal-lavage techniques. An early and a late reaction are detected clinically in the nose after antigen challenge of allergic individuals. In addition, the sensitivity to antigen significantly increases after the initial challenge, and this phenomenon is not obligatorily linked to the presence of a late-phase reaction (LPR). Inflammatory mediators, mostly mast cell- and/or basophil-derived, are detected in the nasal washes and correlate with the symptomatology in both the early and the late reactions. The allergen-induced LPR is marked by an early influx of eosinophils and, later, basophils and neutrophils. Elevation of major basic protein and histamine, but not prostaglandin D₂, is detected during the LPR, giving evidence of active eosinophil and basophil participation. Systemic steroids can effectively suppress the clinical, biochemic, and cellular manifestations of antigen-induced LPR. Topical steroids have a similar effect but are also capable of suppressing the early reaction to antigen. A nonallergic form of rhinitis can be induced in the laboratory by nasal inhalation of dry air at freezing temperatures in individuals who report sensitivity to cold and windy environments. Early and late reactions are also detectable with this stimulus, and the panel of mediators appears to be identical with that of antigen-induced rhinitis, indicating activation of the same cell type(s). This stimulus, however, appears to act through different mechanisms, since pharmacologic agents that control the allergen response are inactive against cold, dry air (CDA) reactions. Studies on the mechanism of CDA-induced rhinitis have detected elevations in the osmolality of nasal secretions after CDA challenge. This occurs only in CDA-sensitive subjects and not in CDA nonresponders or antigen-challenged allergic individuals. Elevated osmolality correlates with mediator release, suggesting a role of nasal fluid tonicity in mast cell activation. The above pieces of information offer significant insight in the mechanisms of allergic and nonallergic inflammation of the nose and the upper airways. Reconstitution of that information into a persuasive model of the naturally occurring disease and development of new therapeutic modalities will be our tasks in the future.