Microglia play a crucial role in the progression of neuroinflammation following traumatic brain injury (TBI). Interleukin-3 (IL-3), a significant regulatory factor, has been involved in the pathogenesis of various diseases, yet its effects on neuroinflammation post-TBI through microglia remain unclear. Here, we evaluate the potential of IL-3 to alleviate neuroinflammation in microglia following TBI. Using the ABplex Multi-Metric Streaming Joint Analysis to detect inflammatory factors, we observed significantly elevated levels of IL-3 in cerebrospinal fluid, but not in blood samples, of patients with headaches and TBI. In addition, we found that administration of exogenous IL-3 within the brain reduced neuroinflammation and promoted functional recovery in rat TBI models. Mechanistically, we identified Peroxiredoxin-1 (PRDX1) as the target of IL-3 in microglia. Notably, the protective effects of IL-3 in TBI rats were abolished when PRDX1 was specifically knocked down in microglia. In conclusion, our experimental research demonstrates that IL-3 acts as a key modulator via regulating microglia polarization to inhibit neuroinflammation. IL-3 improves neurological function and prognosis in TBI rats by recruiting PRDX1 through IL-3R to modulate microglia polarization. Therefore, IL-3 may represent a novel therapeutic strategy for TBI.
Huang et al. (Tue,) studied this question.
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