CCL 23: a new CC chemokine involved in human brain damage

Background CCL 23 role in the inflammatory response after acute brain injuries remains elusive. Here, we evaluated whether CCL 23 blood levels associate with acquired cerebral lesions and determined CCL 23 predictive capacity for assessing stroke prognosis. We used preclinical models to study the CCL 23 homologous chemokines in rodents, CCL 9 and CCL 6. Methods Baseline CCL 23 blood levels were determined on 245 individuals, including ischaemic strokes ( IS ), stroke mimics and controls. Temporal profile of circulating CCL 23 was explored from baseline to 24 h in 20 of the IS . In an independent cohort of 120 IS with a 3‐month follow‐up, CCL 23 blood levels were included in logistic regression models to predict IS outcome. CCL 9/ CCL 6 cerebral expression was evaluated in rodent models of brain damage. Both chemokines were also profiled in circulation and histologically located on brain following ischaemia. Results Baseline CCL 23 blood levels did not discriminate IS , but permitted an accurate discrimination of patients presenting acute brain lesions ( P  = 0.003). IS exhibited a continuous increase from baseline to 24 h in circulating CCL 23 ( P  < 0.001). Baseline CCL 23 blood levels resulted an independent predictor of IS outcome at hospital discharge ( OR adj : 19.702 [1.815–213.918], P  = 0.014) and mortality after 3 months ( OR adj : 21.47 [3.434–134.221], P  = 0.001). In preclinics, expression of rodent chemokines in neurons following cerebral lesions was elevated. CCL 9 circulating levels decreased early after ischaemia ( P  < 0.001), whereas CCL 6 did not alter within the first 24 h after ischaemia. Conclusions Although preclinical models do not seem suitable to characterize CCL 23, it might be a novel promising biomarker for the early diagnosis of cerebral lesions and might facilitate the prediction of stroke patient outcome.