The nucleotide binding domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome/interleukin (IL)-1β axis serves an essential role in regulating the development of rheumatoid arthritis (RA). The dysregulation of cellular metabolism, such as mitochondrial dysfunction, results in the activation of the NLRP3 inflammasome. microRNA (miR)‑33 has previously been identified to be a regulator of lipid metabolism and mitochondrial function. However, whether miR‑33 regulates the NLRP3 inflammasome/IL‑1β axis remains unknown. In the present study, it was observed that an miR‑33 mimic or anti‑miR‑33 markedly stimulated or inhibited, respectively, IL‑1β protein expression levels in mouse peritoneal macrophages. Mechanistically, miR‑33 upregulated the expression of NLRP3 mRNA and protein as well as caspase‑1 activity in primary macrophages. In addition, the results demonstrated that miR‑33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase‑1 activity and IL‑1β secretion. The results of the present study demonstrated that miR‑33 levels and NLRP3 inflammasome activity were increased in peripheral blood monocytes from patients with RA patients compared with healthy donors. In conclusion, the present study identified miR‑33 to be a positive regulator of the NLRP3 inflammasome in macrophages. The miR‑33/NLRP3 inflammasome pathway may therefore be involved in RA development.