Fig 1: Plasma concentrations of CXCL12 [stromal cell-derived factor-1 (SDF-1)], CX3CL1 (fractalkine), and CCL11 (eotaxin-1) in male Wistar rats exposed to ethanol and acute stress. (A) CXCL12 (SDF-1) and (B) CX3CL1 (fractalkine) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle. (C) CCL11 (eotaxin-1) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle with/without acute stress before ethanol exposure. Bars are means and SEM (nanograms per milliliter). CXCL12 and CX3CL1 concentrations were analyzed by Student’s t-test and &&p < 0.01 denotes significant differences compared to the vehicle group. CCL11 concentrations were analyzed by two-way analysis of variance (ANOVA) and **p < 0.01 and ***p < 0.001 denote significant main effect of “stress” and “ethanol exposure,” respectively. (D) CXCL12 (SDF-1); (E) CX3CL1 (fractalkine); and (F) CCL11 (eotaxin-1) concentrations were determined in rats exposed to acute ethanol (3 g/kg, i.g.) at 0, 30, 60, 120, and 240 min after ethanol exposure. Circles are means and SEM (nanograms per milliliter). CXCL12, CX3CL1, and CCL11 concentrations were analyzed by one-way ANOVA and *p < 0.05, **p < 0.01, and ***p < 0.001 denote significant main effect of “time.” +p < 0.05 and ++p < 0.01 denote significant differences compared to t = 0 min. White circles are means and SEM (nanograms per milliliter) at t = 240 min with no ethanol exposure and concentrations were analyzed by Student’s t-test. &p < 0.05 denotes significant differences compared to t = 0 or 240 min with no ethanol.
Fig 2: Brain mRNA expression levels of inflammatory markers, neurotrophic factors, and the α7 nAChR in young, and cognitively unimpaired (AU) or impaired (AI) aged rats. (A-C) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) IL-1β mRNA levels. (D-F) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) MIP-1α mRNA levels. (G-I) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) CX3CL1 mRNA levels. (J-L) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) ICAM-1 mRNA levels. (M-O) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) CNTF mRNA levels. (P-R) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) BDNF mRNA levels. (S-U) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) α7 nAChR mRNA levels. Asterisks mark significant changes in mRNA expression levels compared to young animals: ***P < .001, **P < .01, *P < .05 (univariate ANOVA + post hoc LSD). CHRNA7, α7 nicotinic acetylcholine receptors; BDNF, brain-derived neurotrophic factor; CNTF, ciliary neurotrophic factor; ICAM-1, intercellular adhesion molecule 1; IL-1β, interleukin-1β; MIP-1α, macrophage inflammatory protein 1α.
Fig 3: Effects of repeated cocaine exposure on the relative mRNA expression of Cx3cl1 and Cx3cr1 in the amygdala of rats.Basal Cx3cl1 mRNA levels in male and female control rats at different time points after vehicle administration (fold change vs. males, 2 h) (A). Relative Cx3cl1 mRNA levels in male (B) and female rats (C) 2, 72, and 240 h after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats at different time points after vehicle administration (fold change vs. males, 2 h) (D). Relative Cx3cr1 mRNA levels in male (E) and female rats (F) 2, 72, and 240 h after vehicle or cocaine treatment. Relative mRNA levels were analyzed by two-way ANOVA. Bars represent the mean ± SEM (6–8 rats/group). (^) p < 0.05 and (^^^) p < 0.001 indicate significant differences compared with males. (+) p < 0.05 indicates significant differences compared with control males at 2 h. (*) p < 0.05, (**) p < 0.01, and (***) p < 0.001 indicate significant differences compared with their respective vehicle group. (&&&) p < 0.001 indicates significant differences compared with the vehicle group at 2 h.
Fig 4: Plasma CX3CL1 concentrations in patients with CUD.Plasma CX3CL1 concentrations in CUD patients grouped by the duration of cocaine abstinence (A). Correlation analysis between plasma CX3CL1 concentrations and the duration of cocaine abstinence (days) in all CUD patients (B), men with CUD (C), and women with CUD (D). Data were analyzed using one-way ANOVA (Fig. 6A). Bars represent the mean ± 95 % confidence interval (CI) [control: N = 30 (24 males and 6 females); 0–14 days: N = 28 (7 females and 21 males); 15–30 days: N = 22 (4 females and 18 males); and 31–365 days: N = 38 (8 females and 30 males)]. (***) p < 0.001 indicates significant differences compared with the 0–14 day subgroup, (#) p < 0.05 indicates significant differences compared with the 15–30 day subgroup. The blue arrow and the black dashed lines denote the mean and 95 % CI of CX3CL1 concentrations in the control group. Correlations were assessed using Pearson’s correlation coefficient (r) between log10-transformed days of cocaine abstinence and plasma CX3CL1 concentrations (Fig. 6B, 6C, and 6D). Each dot represents an individual value; the blue line indicates the linear fit, and the black dashed lines indicate the 95 % CI.
Fig 5: Effects of acute cocaine exposure on the relative mRNA expression of Cx3cl1 and Cx3cr1 in the amygdala of rats.Basal Cx3cl1 mRNA levels in male and female control rats 30 min after vehicle administration (fold change vs. males, dose 0) (A). Relative Cx3cl1 mRNA levels in male (B) and female rats (C) 30 min after vehicle or cocaine treatment. Basal Cx3cl1 mRNA levels in male and female control rats 240 min after vehicle administration (fold change vs. males, dose 0) (D). Relative Cx3cl1 mRNA levels in male (E) and female rats (F) 240 min after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats 30 min after vehicle administration (fold change vs. males, dose 0) (G). Relative Cx3cr1 mRNA levels in male (H) and female rats (I) 30 min after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats 240 min after vehicle administration (fold change vs. males, dose 0) (J). Relative Cx3cr1 mRNA levels in male (K) and female rats (L) 240 min after vehicle or cocaine treatment. Basal mRNA levels were analyzed using Student’s t-test. Relative Cx3cl1 and Cx3cr1 mRNA levels were analyzed by one-way ANOVA in male and female rats. Bars represent the mean ± SEM (6–7 rats/group). (^^) p < 0.01 and (^^^) p < 0.001 indicate significant differences compared with control males/dose 0. (*) p < 0.05 and (***) p < 0.001 indicate significant differences compared with the vehicle group. (#) p < 0.05, (##) p < 0.01, and (###) p < 0.001 indicate significant differences compared with the group treated with 5 mg/kg. ($) p < 0.05, ($ $) p < 0.01, and ($ $ $) p < 0.001 indicate significant differences compared with the group treated with 15 mg/kg.
Supplier Page from Abcam for Rat Fractalkine ELISA Kit (CX3CL1)