Objectives: The study clarified whether the T-helper (Th)1/Th2 imbalance existed only in coronary arterial inflammation or in both coronary arterial inflammation and myocardial inflammation and explored the significance of the imbalance of Th1/Th2 function after acute myocardial infarction (AMI).
Background: There are two different inflammatory processes in patients with AMI: the coronary arterial inflammation that leads to the pathogenesis of AMI and the myocardial inflammation after AMI that leads to ventricular remodeling, which are positively and negatively regulated by Th1 and Th2 lymphocytes, respectively.
Methods: Peripheral blood mononuclear cells from 33 AMI patients, 22 unstable angina (UA) patients and splenocytes from 35 AMI Wistar rats were collected. Cytokine-producing Th cells were ambulatorily monitored by 3-color flow cytometry. Interferon (IFN)-gamma and interleukin (IL)-4 mRNA in the rat myocardium and chemokine receptors CCR3,CCR5 and CXCR3 mRNA on the surface of rat T-lymphocytes after AMI were measured by RT-PCR.
Results: IFN-gamma-producing T-cells significantly increased in patients with AMI and UA within 24 hours after the onset of symptom. The high ratio of IFN-gamma-producing T-cells recovered 1 week after the onset in UA patients, while it could be examined 1 week and even 1 month after the onset in AMI patients. The up-regulation of Th1 cell function is consistent with bad heart function. There was no significant difference on the frequencies of IL-4-producing T-cells between each group. 1 week, 2 weeks and 1 month after AMI, IFN-gamma mRNA increased in the myocardium of rats, but there was no significant change on global Th cell functions.
Conclusions: Th1/Th2 functional imbalance exists in both coronary arterial inflammation and myocardial inflammation processes. The up-regulation of Th1 cell-functions may participate in the immune-mediated ventricular remodeling after AMI.