Pathophysiology of reactive airway disease and sinusitis

The association between asthma and sinusitis was recognized more than a century ago. Since 1980, several studies have documented that severe asthma improved after coexisting sinusitis was effectively treated either medically or surgically. Because the mechanism relating sinusitis to asthma is not known, several theories have been proposed: 1) aspiration of infected sinus secretions into the lungs during sleep, 2) enhanced vagal stimulation in the infected sinus producing direct bronchospasm, 3) bronchospasm from excessive airway drying from mouth breathing, 4) production of bacterial toxins that induce partial beta blockade, and 5) production in the infected sinus of cytokines and bronchoconstrictive mediators. There are data to support each of these hypotheses, and any or all of them may be operative. In view of recent demonstrations of activated lymphocytes and eosinophils in asthmatic airways, it is intriguing that biopsies of chronic hypertrophic sinusitis have revealed increased numbers of eosinophils and increased levels of granulocyte-macrophage colony stimulating factor, interleukin-3, and interleukin-5 compared to control tissue. These findings suggest that sinusitis might induce asthma by stimulating eosinophil production and activation and thereby supplying peptidoleukotrienes (LTC4 and LTD 1) and other asthmagenic eosinophil products.