It has been previously reported that hepatitis B e‑antigen (HBeAg) induces microRNA (miR)‑155 expression and promotes liver injury by increasing inflammatory cytokine production in macrophages. Moreover, it was previously demonstrated that miR‑210 alleviates lipopolysaccharide‑stimulated proinflammatory cytokine production in macrophages. In addition, accumulating evidence suggests that miR‑210 is able to suppress hepatitis B virus (HBV) replication in HepG2.2.15 cells. However, it remains unclear whether miR‑210, similar to miR‑155, affects the progress of hepatitis B by regulating macrophage function. Reverse transcription‑quantitative polymerase chain reaction analysis was used to detect miR‑210 levels in serum and cells. HBV‑associated antigens stimulated different types of macrophages and facilitated the observation of the effects of these antigens on miR‑210 expression in macrophages. Co‑culture of peripheral blood monocytes from healthy controls and the serum of patients with chronic hepatitis B (CHB) was conducted to evaluate the effect of HBV‑associated elements in the serum on the expression of the macrophage miR‑210 in vivo. It was observed that miR‑210 expression levels were decreased in the peripheral blood monocytes (PBMs) and serum of patients with CHB and negatively associated with serum alanine aminotransferase and aspartate aminotransferase, but not other clinical parameters including hepatitis B surface antigen (HBsAg), HBeAg, anti‑HBe antibody (HBeAb) and hepatitis B core antibody (HBcAb) and HBV‑DNA. Notably, it was demonstrated that miR‑210 expression was not affected by treatment with HBV‑associated antigens in different types of macrophages. Notably, the serum of patients with CHB was able to markedly downregulate the miR‑210 expression of PBMs in healthy controls. These findings suggested that, unlike the induction of miR‑155 by HBeAg, there may be certain other elements, apart from HBV‑associated antigens, regulating miR‑210 levels in the serum and PBMs of patients with CHB that affect macrophage activation.