Expression of T-cell immunoglobulin- and mucin-domain-containing molecule-1 (TIM-1) is increased in a mouse model of asthma and relationship to GATA-3.

Abstract

It has been suggested that T-cell immunoglobulin-and mucin-domain-containing molecule-1 (TIM-1) plays an important role in the development of allergic asthma, though its molecular mechanism remains unclear. Our aim was to examine the expression of TIM-1 and Th2-associated transcription factor GATA-3 in asthmatic mice, and to evaluate the correlation of TIM-1 and GATA-3 in the pathogenesis of allergic asthma. We examined TIM-1 expression in lung tissue and peripheral blood mononuclear cells (PBMCs) of asthmatic mice by real-time PCR and flow cytometry, respectively; we also investigated TIM-1 and GATA-3 expression in the spleen tissue of asthmatic mice by western blot. These results demonstrate that TIM-1 was significantly increased in pulmonary tissues and PBMCs in asthmatic mice after ovalbumin (OVA) challenge (P<0.05), and that the production of TIM-1 as well as GATA-3 was upregulated in the spleen of asthmatic mice. The production of TIM-1 correlated significantly with the production of GATA-3 in the spleen of asthmatic mice (r=0.753, P<0.05). The results of this study provide the first evidence that increased expression of TIM-1 in asthmatic mice is associated with the Th2-associated transcription factor GATA-3. The findings suggest a possible mechanism for how HAV infection and TIM-1 upregulation influence the development of allergic asthma.