Traumatic brain injury (TBI) is a leading cause of death and disability in persons under age 45. The hallmark secondary injury profile after TBI involves dynamic interactions between inflammatory and metabolic pathways including fatty acids. Omega-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA) have been shown to provide neuroprotective benefits by minimizing neuroinflammation in rodents. These effects have been less conclusive in humans, however. We postulate genetic variants influencing PUFA metabolism in humans could contribute to these disparate findings. Therefore, we sought to (1) characterize the circulating PUFA response and (2) evaluate the impact of rs174537 on inflammation after TBI. A prospective, single-center, observational pilot study was conducted to collect blood samples from Level-1 trauma patients (N = 130) on admission and 24 h post-admission. Plasma was used to quantify PUFA levels and inflammatory cytokines. Deoxyribonucleic acid was extracted and genotyped at rs174537. Associations between PUFAs and inflammatory cytokines were analyzed for all trauma cases and stratified by race (Caucasians only), TBI (TBI: N = 47; non-TBI = 83) and rs174537 genotype (GG: N = 33, GT/TT: N = 44). Patients with TBI had higher plasma DHA levels compared with non-TBI at 24 h post-injury (p = 0.013). The SNP rs174537 was associated with both PUFA levels and inflammatory cytokines (p < 0.05). Specifically, TBI patients with GG genotype exhibited the highest plasma levels of DHA (1.33%) and interleukin-8 (121.5 ± 43.3 pg/mL), which were in turn associated with poorer outcomes. These data illustrate the impact of rs174537 on the post-TBI response. Further work is needed to ascertain how this genetic variant directly influences inflammation after trauma.

中文翻译：

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一项评估 rs174537 对循环多不饱和脂肪酸和创伤性脑损伤患者炎症反应影响的初步研究。

创伤性脑损伤 (TBI) 是 45 岁以下人群死亡和残疾的主要原因。TBI 后的标志性继发性损伤特征涉及炎症和代谢途径（包括脂肪酸）之间的动态相互作用。Omega-3 多不饱和脂肪酸 (PUFA)，如二十二碳六烯酸 (DHA)，已被证明可通过最大限度地减少啮齿动物的神经炎症来提供神经保护作用。然而，这些影响在人类身上的决定性较小。我们假设影响人类 PUFA 代谢的遗传变异可能导致这些不同的发现。因此，我们试图 (1) 表征循环 PUFA 反应和 (2) 评估 rs174537 对 TBI 后炎症的影响。一个前瞻性的、单中心的、进行了观察性试点研究，以收集入院时和入院后 24 小时的 1 级创伤患者 (N = 130) 的血样。血浆用于量化 PUFA 水平和炎性细胞因子。提取脱氧核糖核酸并在 rs174537 进行基因分型。分析了所有创伤病例的多不饱和脂肪酸和炎性细胞因子之间的关联，并按种族（仅限白种人）、TBI（TBI：N = 47；非 TBI = 83）和 rs174537 基因型（GG：N = 33，GT/TT：N）分层= 44). 与非 TBI 患者相比，TBI 患者在受伤后 24 小时具有更高的血浆 DHA 水平（分析了所有创伤病例的多不饱和脂肪酸和炎性细胞因子之间的关联，并按种族（仅限白种人）、TBI（TBI：N = 47；非 TBI = 83）和 rs174537 基因型（GG：N = 33，GT/TT：N）分层= 44). 与非 TBI 患者相比，TBI 患者在受伤后 24 小时具有更高的血浆 DHA 水平（分析了所有创伤病例的多不饱和脂肪酸和炎性细胞因子之间的关联，并按种族（仅限白种人）、TBI（TBI：N = 47；非 TBI = 83）和 rs174537 基因型（GG：N = 33，GT/TT：N）分层= 44). 与非 TBI 患者相比，TBI 患者在受伤后 24 小时具有更高的血浆 DHA 水平（p  = 0.013）。SNP rs174537 与 PUFA 水平和炎性细胞因子相关 ( p  < 0.05)。具体而言，具有 GG 基因型的 TBI 患者表现出最高的 DHA (1.33%) 和白细胞介素 8 (121.5 ± 43.3 pg/mL) 血浆水平，这反过来又与较差的结果相关。这些数据说明了 rs174537 对 TBI 后反应的影响。需要进一步的工作来确定这种遗传变异如何直接影响创伤后的炎症。