Fig. 5: CpE@BMV effectively suppresses E. coli pulmonary infection in vivo.

a Experimental scheme of the E. coli-induced pulmonary infection model in female BALB/c mice. Different formulations administered via tracheal needle on days 1, 2, 3, and 6 using equivalent doses of Cip, Ea, and BMV were 1.76 mg/kg, 0.76 mg/kg, and 1.12 mg/kg, respectively (n = 4 biologically independent mice). b Quantified c.f.u. of E. coli in excised lung tissues from treatment endpoints was performed (n = 4 biologically independent mice). c Representative H&E staining images of the collected lung tissues from different groups after various treatments on day 7. Each experiment was repeated three times independently with similar results. d, e Representative scatter plots of flow cytometry data and quantitative results demonstrated the percentage of M1-phenotype macrophages (d) and M2-phenotype macrophages (e) within the CD11b⁺F4/80⁺ cell population in the lung tissues on day 7 after various treatments (n = 4 biologically independent mice). f Representative immunofluorescent images were captured for lung tissues. Each experiment was repeated three times independently with similar results. g–k Representative scatter plots of flow cytometry data and quantitative results showing the number of mature DCs (CD80⁺CD86⁺) (g), CD8⁺ T cells (CD3⁺CD8⁺) (h), CD4⁺ T cells (CD3⁺CD4⁺) (i), regulatory T cells (CD3⁺CD4⁺Foxp3⁺) (j), plasmablasts (CD138⁺CD19⁺) and plasma cells (CD138⁺CD19⁻) (k) (n = 4 biologically independent mice). l–o Cytokine concentrations of TNF-α (l), IL-6 (m), IL-1β (n), and IL-10 (o) in the infected lung tissue from the mice that received various treatments as measured by ELISA (n = 4 biologically independent mice). Data are presented as means ± s.d. Statistical significance was determined using one-way ANOVA with Tukey’s post hoc test, p > 0.05, no significance (ns), *p < 0.05; **p < 0.01; ***p < 0.001; and ****p < 0.0001.