Elevated expression of messenger ribonucleic acid encoding IL-13 in the bronchial mucose of atopic and nonatopic subjects with asthma

Local secretion of cytokines by T cells within the bronchial mucosa, with consequent selective eosinophil influx, has been implicated in the pathogenesis of bronchial asthma, The cytokine IL-13 exhibits activities (selective eosinophil vascular adhesion by very late antigen-4/vascular cell adhesion molecule-1 interaction and promotion of IgE synthesis and ''T-H2-type'' T cell responses) that may be relevant to this process, We hypothesized that, compared with conditions in control subjects, elevated expression of messenger ribonucleic acid (mRNA) encoding IL-13 is a feature of the bronchial mucosa of both atopic (positive skin prick test result to at least one of a range of common aeroallergens) and nonatopic (negative skin prick test results and serum total IgE concentrations within the normal range) subjects with asthma, With use of a semiquantitative reverse transcriptase-polymerase chain reaction technique, we measured the quantities (relative to beta-actin) of IL-13 mRNA in bronchial mucosal biopsy specimens from atopic and nonatopic subjects with asthma and atopic and nonatopic control subjects. Biopsy specimens from the subjects with asthma, whether the subjects were atopic or nonatopic, had statistically equivalent quantities of IL-13 mRNA relative to beta-actin, and these quantities were significantly elevated compared with those in specimens from both the atopic and nonatopic control subjects (p less than or equal to 0.02 in each case), in which the quantities of IL-13 mRNA relative to beta-actin were also statistically equivalent, The quantities of IL-13 mRNA reflected the numbers of EG2+ eosinophils per unit area of submucosa in the biopsy specimens as determined by immunohistochemistry, which were statistically equivalent in the atopic and nonatopic subjects with asthma and significantly elevated as compared with those in both the atopic and nonatopic control subjects without asthma (p less than or equal to 0.007 in each ease), Taking the subjects with asthma as a group, no correlations were observed between the quantities of IL-13 mRNA (relative to p-actin) and several measures of disease severity. These data are consistent with the hypothesis that IL-13 plays a role in the pathogenesis of both atopic and nonatopic asthma, at least partly through promoting recruitment of eosinophils to the bronchial mucosa, although ether factors mag be more important in regulating the severity of the disease.