Fig 1: Th1 responses induced by the B.1.1.7 monovalent, B.1.351 monovalent and SCTV01C bivalent vaccines. (A) Scheme of immunization and tissue processing. C57BL/6J mice (n = 8/group) were immunized with B.1.1.7 monovalent vaccine (1 μg/dose), B.1.351 monovalent vaccine (1 μg/dose), or SCTV01C (1 μg/dose for each antigen) on days 0, 14 and 28. Splenocytes from immunized mice were stimulated with SARS-CoV-2 spike protein S polypeptides on day 42. (B) Number of IFN-γ (Th1 cytokine) and IL-4 (Th2 cytokine) positive Spot-forming cells (SFC) was evaluated. (C) Th1 (IFN-γ, IL-2) and Th1 (IL-4, IL-5 and IL-13) cytokines in culture supernatants from S peptides-stimulated mouse splenocytes were measured by flow cytometry. The results are representative of 3 independent experiments. Vac is an abbreviation for Vaccine. Bars show mean ± SD.
Fig 2: Time course of hippocampal pro-inflammatory cytokine responses following systemic LPS administration. (A-D) Mice (n = 5-7) were injected (i.p.) with LPS (1 mg/kg), and hippocampal samples were collected at 2, 4, 6, 8, and 24 h post-injection. Control mice received saline injection (i.p.) and samples were collected 2 h later. Pro-inflammatory cytokine levels (IL-6, TNF-α, IFN-γ and IL-5) were quantified using a multiplex bead-based assay. Statistical analysis was performed using one-way ANOVA (A: F[5,35] = 16.62, p < 0.001; B: F[5,35] = 3.41, p < 0.05; C: F[5,35] = 4.94, p < 0.01; D: F[5,34] = 3.61, p < 0.01) with Bonferroni post-hoc tests (*p < 0.05, **p < 0.01, ***p < 0.001). Data are presented as mean ± SEM
Fig 3: DOI pretreatment on hippocampal anti-inflammatory cytokine responses following LPS administration in WT and 5-HT2AR-KO mice. (A-D) Mice (n = 5-13) were pretreated (i.p.) with DOI (0.3 or 1 mg/kg) or saline 24 h prior to LPS (1 mg/kg, i.p.) or saline, and hippocampi were collected 4 h after LPS/saline injection. Anti-inflammatory cytokine levels (IL-4, IL-10, IL-13 and IL-2) were quantified using a multiplex bead-based assay. Statistical analysis was performed using one-way ANOVA (A: WT F[3,38] = 0.20, p > 0.05 and KO F[3,21] = 5.33, p < 0.01; B: WT F[3,37] = 1.01, p > 0.05 and KO F[3,21] = 4.31, p < 0.05; C: WT F[3,38] = 1.33, p > 0.05 and KO F[3,22] = 1.52, p > 0.05; D: WT F[3,39] = 2.33, p > 0.05 and KO F[3,21] = 1.15, p < 0.05) with Bonferroni post-hoc tests (*p < 0.05, n.s., not significant) and two-way ANOVA (A: treatment F[3,59] = 1.21, p > 0.05, genotype F[1,59] = 8.06, p < 0.01, interaction F[3,69] = 2.11, p > 0.05; B: treatment F[3,58] = 1.14, p > 0.05, genotype F[1,58] = 0.01, p > 0.05, interaction F[3,58] = 1.14, p > 0.05; C: treatment F[3,60] = 1.25, p > 0.05, genotype F[1,60] = 0.51, p > 0.05, interaction F[3,60] = 1.11, p > 0.05; D: treatment F[3,60] = 1.55, p > 0.05, genotype F[1,60] = 0.03, p > 0.05, interaction F[3,60] = 1.72, p > 0.05) with Bonferroni post-hoc tests. Data are presented as mean ± SEM
Fig 4: Correlation between hippocampal cytokine levels and immobility time in the FST. (A-E) Correlation between IL-6 (A), TNF-α (B), IL-4 (C), IL-13 (D), and IL-2 (E) and immobility time in the FST (n = 20). Individual data points are color-coded by treatment group, as indicated in the legend. Correlation analysis was conducted using Pearson’s r
Fig 5: DOI pretreatment on hippocampal pro-inflammatory cytokine responses following LPS administration in WT and 5-HT2AR-KO mice. (A-D) Mice (n = 4-13) were pretreated (i.p.) with DOI (0.3 or 1 mg/kg) or saline 24 h prior to LPS (1 mg/kg, i.p.) or saline, and hippocampi were collected 4 h after LPS/saline injection. Pro-inflammatory cytokine levels (IL-6, TNF-α, IFN-γ and IL-5) were quantified using a multiplex bead-based assay. Statistical analysis was performed using one-way ANOVA (A: WT F[3,39] = 17.52, p < 0.001 and KO F[3,22] = 8.75, p < 0.001; B: WT F[3,37] = 7.40, p < 0.001 and KO F[3,21] = 5.13, p < 0.01; C: WT F[3,26] = 0.15, p > 0.05 and KO F[3,21] = 5.58, p < 0.01; D: WT F[3,26] = 0.19, p > 0.05 and KO F[3,21] = 4.39, p < 0.05) with Bonferroni post-hoc tests (*p < 0.05, **p < 0.01, ***p < 0.001, n.s., not significant) and two-way ANOVA (A: treatment F[3,61] = 22.23, p < 0.001, genotype F[1,61] = 23.85, p < 0.001, interaction F[3,61] = 4.23, p < 0.01; B: treatment F[3,58] = 12.61, p < 0.001, genotype F[1,58] = 9.10, p < 0.01, interaction F[3,58] = 2.77, p < 0.05; C: treatment F[3,47] = 0.74, p > 0.05, genotype F[1,47] = 3.45, p = 0.06, interaction F[3,47] = 1.17, p > 0.05; D: treatment F[3,47] = 0.51, p > 0.05, genotype F[1,47] = 6.08, p < 0.05, interaction F[3,47] = 1.47, p > 0.05) with Bonferroni post-hoc tests (+p < 0.05, ++p < 0.01). Data are presented as mean ± SEM
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