The effects of IL-32 on the inflammatory activation of cultured rat primary astrocytes

A new family of cytokine IL-32 has been implicated in pro-inflammatory immune responses several human diseases such as rheumatoid arthritis, inflammatory bowel diseases and vasculitis. In this study, we investigated the role of IL-32 in the inflammatory activation of cultured rat primary astrocytes. Treatment of IL-32 increased ROS production and augmented lipopolysaccharide-induced increased production of nitric oxide as well as the expression of iNOS. IL-32 also induced the expression of MMP-9 but not MMP-2 in rat primary astrocytes. The increased expression of these inflammatory mediators was accompanied by the increased mRNA expression encoding iNOS, MMP-9 and TNF-α. ERK1/2 and p38, two essential regulators of pro-inflammatory signaling in rat primary astrocytes were activated by IL-32 as evidenced by increased phosphorylation. The results from the present study suggest that IL-32 may play a role in the regulation of neuroinflammatory responses in several neurological disease conditions such as ischemia and Alzheimer’s disease.

Research highlights
► IL-32 synergistically increases NO and ROS production in LPS-stimulated rat primary astrocytes.
► IL-32 induces proinflammatory mediators such as iNOS, MMP-9 and TNF-α.
► IL-32 activates ERK1/2 and p38 signaling that might underlie the proinflammatory action of IL-32.
► IL-32 may modulate neuroinflammatory responses in neurological diseases.