Obesity and hypertension are major risk factors for cardiovascular diseases that affect millions of people worldwide [1], [2], [3]. Both conditions are associated with chronic low-grade inflammation, which is mediated by various cytokines [4], [5], [6], [7].

Interleukin-6 (IL-6) is a pleiotropic cytokine that has both pro-inflammatory and anti-inflammatory effects depending on the context. Traditionally, IL-6 is considered a pro-inflammatory cytokine as it promotes neutrophilia and TH17 T cell differentiation while blocking regulatory T cell (T reg) differentiation, contributing to the pathophysiology of several inflammatory diseases [8]. However, an immunoregulatory role for IL-6 has also been suggested in specific contexts. For instance, genetic deficiency of IL-6 increases inflammatory responses to local and systemic endotoxin administration [9]. And muscle-derived IL-6 may also mediate some of the anti-inflammatory and insulin-sensitizing effects of physical exercise [10].

Some studies suggest that IL-6 promotes vascular inflammation and contributes to the development of obesity-hypertension, while others indicate that IL-6 has immunoregulatory and insulin-sensitizing effects that may protect against obesity-hypertension [11]. Obesity is proven to be a positive modulator of Interleukin-6(IL-6) and IL-6 receptor (IL-6R) expression in the adipose tissue which might be a contributory mechanism to induce metabolic inflammation [12]. Also, IL-6 causes vascular inflammation by promoting smooth muscle cell (SMC) proliferation and migration, impairing endothelial function, and attracting and activating inflammatory mediators. This results in atherosclerotic plaque formation and instability, which raise the risk of obesity-hypertension [13], [14], [15].

Alternatively, in animals, inhibition of IL-6 attenuates the salt-sensitive hypertension, and deletion of IL-6 can inhibit the Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) pathway, reduce Ang II-induced hypertension, and lower mean arterial pressure [9], [16], [17]. Lifetime deficiency of IL-6 may also disrupt the balance between IL-6 and IL-10 and promote atherosclerosis [18], [19].

However, the exact role of IL-6 in obesity-associated hypertension needs to be lucubrated. A large number of studies have suggested that IL-6 can have different effects depending on the cell or tissue context and the type of IL-6 receptor involved [7], [20], [21]. IL-6 signaling is mediated by a complex of IL-6, the transmembrane IL-6 receptor (mIL-6R) or soluble IL-6R (sIL-6R), and the signal-transducing subunit gp130 [8], [22]. Therefore, three modes of IL-6 signaling may occur: IL-6 binding to mIL-6R (classic), to sIL-6R (trans-signaling), or to gp130 on nearby cells via IL-6R (trans-presentation) [8], [22]. Then, it is important to investigate the diverse role of IL-6 in obesity-hypertension using various experimental settings.

In this study, we aimed to examine the relationship between serum IL-6 concentrations and various anthropometric and biochemical parameters in four subgroups of Chinese adults: normal healthy group (NH), just obesity group (JO), just-hypertension group (JH), and obesity-hypertension group (OH). We hypothesized that serum IL-6 concentrations would vary among the four subgroups and correlate with different parameters based on the presence or absence of obesity and hypertension. We also explored the predictors of serum IL-6 concentrations in each subgroup using multiple regression analysis. Our study may provide new insights into the colorable role of IL-6 in obesity-hypertension and its implications for diagnosis and treatment.