Chronic alcohol consumption induces cardiac remodeling in mice from Th1 or Th2 background

AimsThe effects of T helper (Th) cells on alcoholic cardiomyopathy have not been extensively investigated. Strain of mice with Th1 or Th2 immunological background were utilized in this study in order to explore the role of Th1/Th2 in chronic alcohol-induced cardiac fibrosis.Methods and resultsC57BL/6 WT or Balb/c mice were treated with alcohol for 90 days. Then cardiac structure and function were analyzed via echocardiography. Spleen CD4 + CD25 + Foxp3+ Tregs were determined by flow cytometry. The hearts were stained using haematoxylin and eosin (HE) and Masson's trichome. Myocardial ultrastructure was observed by electron microscopy. Expression of T-bet, GATA-3, IL-4 and IFN-gamma were determined by real-time RT-PCR. The heart was dilated significantly in the C57BL/6 WT + alcohol group and Balb/c + alcohol group compared with the controls. CD4 + CD25 + Foxp3+ Tregs were not statistically different. Masson's trichome staining revealed that fibrosis was more pronounced in the alcohol treated groups than the controls. Fibrosis was more evident in the Balb/c + alcohol group compared to the C57BL/6 WT + alcohol group. Alcohol consumption caused a decrease in the Th1 poalrization and an increase in the Th2 response.ConclusionsChronic alcohol consumption induced a Th2 response within the Th1/Th2 balance. Th2 response is one of the underlying mechanism involved in alcohol-induced cardiac fibrosis.

► Fibrosis was more evident in the Balb/c+alcohol group compared to the C57BL/6 WT+alcohol group.
► Alcohol consumption caused a decrease in the Th1 polarization and an increase in the Th2 response.
► Th2 response is one of the underlying mechanism involved in alcohol-induced cardiac fibrosis.