Allergic Asthma May Diminish Healthy Immune Response to Respiratory Viruses

Emma Hitt, PhD

June 07, 2010

June 7, 2010 — Allergic asthma may diminish the immune response to respiratory viruses such as influenza, according to new research findings.

Michelle A. Gill, MD, PhD, from the Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, and colleagues reported the findings, which appeared in the June 1 issue of the Journal of Immunology.

"Our findings imply that the better your asthma is controlled, the more likely you are to have an appropriate response to a virus," noted Dr. Gill in a written release.

"Respiratory viral infections are common precipitants of asthma exacerbations," Dr. Gill and colleagues note in the article. A definitive link between diminished antiviral responses and dendritic cells in patients with these diagnoses has not yet been established; consequently, the researchers sought to determine whether allergic phenotype influences antiviral responses, using a model of allergic asthma.

The study included 56 participants, aged 3 to 35 years, of whom 26 suffered from allergic asthma. The remainder served as a control. Those in the allergic asthma group also had a positive skin test to at least one indoor allergen.

Researchers isolated dendritic cells from study participants and found that when exposed to the influenza virus, the cells of those with allergic asthma produced diminished levels of interferon-alfa compared with those of control participants. They also found that TLR-7, a cell protein that recognizes the RNA of respiratory viruses and triggers production of interferon, was not upregulated as much in allergic asthma patients as in control patients. In addition, there was also a loss of upregulation of plasma dendritic cell maturation/costimulatory molecules in participants with allergic asthma.

The researchers speculate that the immune-suppressing effect of the allergic stimulation of dendritic cells might be related to the high levels of IgE expressed in people with allergic asthma. Among the patients participating in this study, elevated IgE levels were associated with impaired capacity of dendritic cells to produce interferon when exposed to influenza.

According to Dr. Gill, these findings suggest that when the cold/influenza and allergy seasons collide, the immune response in individuals with allergic asthma may worsen their disease. "These findings [may] imply that allergic triggers associated with exposure to indoor allergens like pet dander and dust mites can potentially render cells deficient in responding to a virus," she said. They also explain why people with allergic asthma may experience asthma exacerbations when they acquire respiratory viral infections.

At this time, an investigation is ongoing to determine whether suppression of IgE in allergic asthma patients will improve response of dendritic cells to allergens and respiratory viruses.

Independent commentator Louis Rosenthal, PhD, from the University of Wisconsin School of Medicine and Public Health, Madison, noted that these findings are significant because they "describe a novel mechanism by which antiviral defenses could be compromised in patients with allergic asthma." In addition, the findings suggest that "blunting allergic manifestations in asthma patients might have the added benefit of boosting the ability of the immune system to effectively handle viral respiratory infections, which are the main cause of asthma exacerbations," he told Medscape Allergy & Clinical Immunology.

According to Dr. Rosenthal, the results of this study also provide additional impetus for investigating whether clinical interventions aimed at reducing allergen-specific IgE levels, such as specific immunotherapy or treatment with the anti-IgE antibody omalizumab, might reduce the incidence of virus-induced asthma exacerbations, at least in patients with high levels of IgE.

The study was funded by a grant from the Exxon Mobil Corporation and from the National Institutes of Health. The authors and commentator have disclosed no relevant financial relationships.

J Immunol. 2010;184:5999-6006. Abstract


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