Correlation of acetyl-coenzyme A carboxylase 1 with Th17 and Th1 cells, serving as a potential prognostic biomarker for acute ischemic stroke patients

Background Acetyl-coenzyme A carboxylase 1 (ACC1) regulates lipid homeostasis, T helper (Th) cell differentiation, oxidative stress, inflammation response, and neurological process, engaging in acute ischemic stroke (AIS) pathogenesis, while its clinical utility in AIS is unclear. Hence, this study intended to explore the correlation among blood ACC1, Th17, and Th1 cells, and ACC1's potency as a prognostic biomarker for AIS management. Methods ACC1 in peripheral blood mononuclear cells (PBMCs) of 160 AIS patients and 30 controls were determined using RT-qPCR; blood Th17 and Th1 cells in AIS patients were quantified by flow cytometry. Results ACC1 was increased in AIS patients compared with controls (median (interquartile range): 2.540 (1.753-3.548) vs. 0.980 (0.655-1.743), p < 0.001), which exhibited a good value to reflect AIS risk with the area under the curve of 0.872 (95% CI: 0.805-0.939). Moreover, ACC1 was positively linked with Th17 (r = 0.374, p < 0.001) and Th1 (r = 0.178, p = 0.024) cells in AIS patients. Additionally, ACC1 (r = 0.328, p < 0.001), Th17 (r = 0.272, p = 0.001), and Th1 cells (r = 0.195, p = 0.014) were positively associated with the National Institutes of Health Stroke Scale score in AIS patients. ACC1 high vs. low (p = 0.038) and Th17 high vs. low (p = 0.026) were related to shortened recurrence-free survival (RFS) in AIS patients, while Th1 cells (p = 0.179) were not correlated with RFS. Whereas ACC1 (p = 0.248), Th17 (p = 0.079), and Th1 cells (p = 0.130) were not linked with overall survival (OS) in AIS patients. Conclusion Circulating ACC1 overexpression correlates with increased Th17, Th1 cells, NIHSS score, and shortened RFS in AIS patients.

Automated summary

The study revealed that the overexpression of circulating ACC1 in AIS patients is associated with increased Th17 and Th1 cells, NIHSS score, and shortened recurrence-free survival.