Uric acid (UA) has a multifaceted role, such as antioxidant, pro-oxidative, pro-inflammatory, nitric oxide modulating, anti-aging, and immune effects, which are significant in physiological and pathological contexts [1]. Uric acid is a heterocyclic organic compound that is the final product of purine synthesis in the human body. This process can occur using purine precursors supplied with food as substrates and those derived from the decomposition of endogenous compounds, i.e., nucleic acids or nucleotides released from damaged cells [2]. UA has antioxidant activity by capturing free radicals and chelating metal ions. This compound occurs mainly in the endothelial cells of the liver, intestines, kidneys, and vessels. It is removed from the body by excretion through the kidneys (approximately 70% of daily production) and intestines (the remaining approximately 30%), using, among others, the intestinal microbiota [3]. The condition in which the concentration of uric acid in serum exceeds 7.0 mg/dl is called hyperuricemia. It can lead to gout development, characterized by the deposition of urate crystals in the joints and attacks of severe pain [4]. So far, few other phenomena, apart from the aforementioned disease, have been associated with increased uric acid concentration. Still, in recent years, many studies have shown the relationship between hyperuricemia and the development of diseases falling within the scope of various fields of medicine [5,6,7].

The factor that connects the mechanisms of hyperuricemia’s influence on the etiopathogenesis of diseases is the participation of uric acid in the development of the inflammatory reaction and, above all, the activation of immune system cells resulting from this condition. High uric acid concentrations stimulate the synthesis of proinflammatory cytokines, including TNF-, IL-1, and IL-6. Increased production of cytokines then triggers the activation of immune cells, which participate in the immunological mechanisms that are components of the disease process [6, 7]. It has also been shown that uric acid crystals significantly induce the production of IL-1β by acting on neutrophils previously exposed to IL-6 and activating the NLRP3 inflammasome (pyrin domain of the NLR family) [8]. Moreover, evidence indicates that hyperuricemia-induced dysbiosis and intestinal-barrier impairment amplify the IL-1β/IL-6-driven NLRP3 inflammatory cascade, thereby sustaining systemic low-grade inflammation [9]. Interestingly, the findings of a cross-sectional study conducted by Yang et al. suggest that the high-sensitivity C-reactive protein (hsCRP) level is positively associated with the prevalence of hyperuricemia [10]. However, there is insufficient research to determine whether modulating uric acid levels can change the inflammatory response in coexisting diseases, including those associated with increased inflammatory markers.

Interleukin 6 (IL-6) is a multifunctional cytokine that is key in regulating the body’s immune response, inflammatory processes, and homeostasis. Produced mainly by macrophages, monocytes, fibroblasts, and endothelial cells in response to infections, injuries, or other inflammatory stimuli, IL-6 plays a signaling role, affecting many cell types [11]. In the immune system, IL-6 stimulates the maturation of B lymphocytes into plasma cells capable of producing antibodies and supports the differentiation of T lymphocytes, primarily the Th17 population, which are essential in the antibacterial response and the development of autoimmune diseases. This cytokine also plays a vital role in the acute phase response–it stimulates hepatocytes to synthesize proteins such as CRP, fibrinogen, or serum amyloid A, which are indicators of inflammation [12].

Interleukin 1 beta (IL-1β) is one of the key pro-inflammatory cytokines, playing an essential role in initiating and maintaining the body’s inflammatory response. It is produced mainly by monocytes, macrophages, and dendritic cells in response to infectious stimuli, tissue damage, or other stress factors. Active IL-1β acts as a potent mediator of the inflammatory response–it stimulates endothelial cells to express adhesion molecules that enable leukocyte migration to sites of inflammation. Also, it induces the secretion of other cytokines and chemokines. It also affects the central nervous system, causing an increase in body temperature (fever) by acting on the hypothalamus. IL-1β also activates T and B lymphocytes to differentiate antigen-presenting cells, making it an essential element of the innate and adaptive response [13]. Recent evidence shows IL-1β activation in hyperuricemia-associated ocular inflammation [14].

Serum uric acid levels in the context of inflammation-related diseases can also be used in diagnostics. It has been proven that in patients with gout, high UA levels positively correlate with levels of proinflammatory cytokines such as TNF-, IL-6, and C-reactive protein (CRP). Simultaneous determination and comparison of the above-mentioned substances’ values can increase the accuracy of gout diagnostics [15].

Uric acid balance appears essential for older adults’ health and functioning [16]. Developing efficient diagnostic and treatment methods to reduce the risk of diseases associated with its excess can be aided by knowledge of its effects on the body. The current investigation was designed to determine the relationship between uric acid levels and selected interleukins (IL-6 and IL-1β) quantified in older inpatients. The present contribution aimed to explore whether the different uric acid levels resulting from properly treated, unsuccessfully treated, or untreated hyperuricemia influence the immune response, using the aforementioned interleukins.