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The Impact of Upper Airway Allergic Inflammation on Asthma

The Allergist's Perspective on Allergic Rhinitis and Asthma

William W. Busse, M.D.
University of Wisconsin
Madison, Wisconsin

Many patients with allergic rhinitis have co-existing asthma, and an exacerbation of nasal allergic symptoms can enhance lower airway symptoms and further alter existing pulmonary physiology. There is considerable evidence that this association exists (Corren et al., J Allergy Clin Immunol 1992; 89:611-618; Madonini et al., J Allergy Clin Immunol 1987; 79:358-363; Watson et al., J Allergy Clin Immunol 1993; 91:97-101). In addition, clinical studies have shown that treatment of allergic rhinitis with inhaled corticosteroid will diminish later airway symptoms. Thus, there appears to be a “link” between upper airway allergic disease and allergic events in the lower airway. The mechanisms underlying this connection are not fully established. In addition, the association between upper airway allergic processes and events in the lower airway can be further enhanced by the presence of a viral respiratory illness. The interaction of a viral respiratory infection in the nose and co-existing inflammatory reactions in the lung will be the focus of this discussion.

In both children and adults, viral upper respiratory infections can provoke asthma. The infection most likely to provoke these asthma exacerbations is the common cold virus, rhinovirus (Johnston et al., BMJ 1995; 310:1225-1228). A number of studies have found the co-existence of allergic rhinitis to be a risk factor for wheezing with a cold (Rakes et al., Am J Respir Crit Care Med 1999; 159:785-790). Moreover, in studies employing an experimental infection of rhinovirus, the prevalence of allergic rhinitis and allergic asthma enhances the likelihood that a rhinovirus cold will increase the bronchial responsiveness. Because the rhinovirus tends to primarily infect the upper airway, there appears to be a link between allergic and infectious processes in the nose and the lung.

A number of models have been used to determine the mechanisms by which respiratory viruses provoke asthma. What has been learned is the following:

  1. Upper respiratory infections enhance the likelihood that an inhaled antigen challenge will provoke a late-phase inflammatory response (Lemanske et al., J Clin Invest 1989; 83:1-10).

  2. A rhinovirus respiratory infection can enhance pulmonary mast cell mediator release to antigen and enhance eosinophil recruitment to the lung (Calhoun et al., J Clin Immunol 1994; 94:2200-2208).

  3. There is evidence that some patients with allergic rhinitis and asthma have a diminished generation of interferon-γ to virus, which intensifies the symptoms of a cold (Gern et al., Am J Respir Crit Care Med 2000; 162:2226-2231).

Collectively, these data indicate that allergic rhinitis is a risk factor for respiratory viruses provoking asthma, and that these events in the nose will initiate lower airway allergic processes. Furthermore, there appears to be a difference in the generation of interferon-γ in allergic rhinitis subjects, and this difference promotes the likelihood of an infection, its severity and persistence.

Slide presentation

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