The cytokine interleukin-1 (IL-1) may contribute to regulation of inflammatory processes, apoptosis or contractility in heart cells. The stimulation of functions by both agonistic isoforms IL-1α and IL-1β can be modified by the IL-1 receptor antagonist (IL-1ra), by the IL-1 receptors or by regulation of IL-1β maturation through caspase-1. Data concerning endogenous production of IL-1 and proteins regulating IL-1 functions in heart are limited. Thus, we investigated expression and function of IL-1 in cultured neonatal rat heart cells as well as expression of IL-1α, IL-1β, IL-1ra, IL-1 receptor type I (IL-1-RI), caspase-1 and caspase-3 in tissues derived from human heart. We showed that cultured neonatal rat cardiomyocytes expressed IL-1α mRNA, IL-1α protein and cell-associated IL-1α activity. Biologically active IL-1α was present at the cell surface of the cardiomyocytes. Although this cells expressed IL-1β mRNA, we did not find IL-1β protein cell-associated and in the supernatants of cultured cardiomyocytes. Analysis of commercially available human heart tissues showed that human fetal cardiac tissue, but not human adult tissue expressed detectable IL-1α mRNA. Likewise, IL-1α mRNA was not detected in the tissues of patients with dilated (DCM) and ischemic (ICM) cardiomyopathy as well as in donor hearts used as a control. We showed, that the expression of the IL-1β, IL-1-RI, caspase-1 and caspase-3 was the same in both patients groups and in the control group. On the other hand, the total IL-1ra mRNA expression was significantly decreased in tissues of DCM patients, as compared to ICM patients and control. The expression of functional active IL-1α on the cell surface of neonatal rat cardiomyocytes suggests a role of this cytokine in regulation of cellular functions in the neonatal heart. Our further data provide evidence for a lowered IL-1ra mRNA expression in the heart of DCM patients and indicate that IL-1ra could participate in DCM pathogenesis, probably by provoking the imbalance of IL-1ra and IL-1 in cardiac tissues.