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1 Laboratoy of Respiration Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; Physiology Program, Harvard School of Public Health, Boston, MA, USA
2 Physiology Program, Harvard School of Public Health, Boston, MA, USA
3 Pulmonary, Allergy and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.
The chemokine thymus- and activation-regulated chemokine (TARC) induces selective migration of Th2, but not Th1 lymphocytes and is upregulated in the airways of asthmatic patients. The purpose of this study was to determine whether human airway smooth muscle (HASM) cells produce TARC. Neither IL-4, IL-13, IL-1
, IFN
, nor TNF
alone stimulated TARC release into the supernatant of cultured HASM cells. However, both IL-4 and IL-13 increased TARC protein and messenger RNA expression when administered in combination with TNF but not IL-1 or IFN. Macrophage-derived chemokine was not expressed under any of these conditions. TARC release induced by TNF plus IL-13 or TNF plus IL-4 was inhibited by the -agonist isoproterenol, and by other agents that activate protein kinase A, but not by dexamethasone. To determine whether polymorphisms of the IL-4R impact the ability of IL-13 or IL-4 to induce TARC release, HASM cells from multiple donors were genotyped for the Ile50Val, Ser478Pro, and Gln551Arg polymorphisms of the IL-4R. Our data indicate that cells expressing the Val50/Pro478/Arg551 haplotype had significantly greater IL-13 or IL-4 induced TARC release than cells with other IL-4R genotypes. These data indicate that Th2 cytokines enhance TARC expression in HASM cells in an IL-4R genotype dependent fashion, and suggest that airway smooth muscle cells participate in a positive feedback loop that promotes the recruitment of Th2 cells into asthmatic airways.
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