Inflammatory stimuli are usually associated with homeostatic responses, which have an important function in protecting the body from excessive inflammatory damage. Previous studies reported the anti-inflammatory effect of miR-181a. The current study utilized two animal models of inflammation, induced by either lipopolysaccharides (LPS) or streptozotocin. We demonstrated that inflammatory stimuli significantly increase miR-181a expression, concurrently with inflammatory factors. In addition, the knock down of toll-like receptor 4 (TLR-4) by small interfering RNA in LPS-induced Raw264.7 cells significantly reduces the expression of both miR-181a and inflammatory factors. Furthermore, patients with inflammatory response show increased expression of miR-181a, which is strongly correlated with the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha. These data indicate that the up-regulation of miR-181a may be associated with homeostatic response to inflammatory stimuli by TLR-4 pathway activation. Therefore, miR-181a may serve as a novel marker for inflammatory response.
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