Figure 4.

3-IAld promotes resistance to VVC by inducing the IL-22/IL-18 axis via AhR. (A) IL-22, IL-1β production (pg/mg, cytokine/total proteins for each sample), and (B) fungal growth (mean log CFUs ± s.e.m.) at 7 dpi in vaginal fluids of C57BL/6 mice (n = 6 mice/group) inoculated with 5 × 10⁶ C. albicans blastoconidia and treated subcutaneously (sc), intraperitoneally (ip), or intragastrically (ig) with 3-IAld every day starting the day of infection. (C) C57BL/6 and Ahr^−/− mice (n = 6 mice/group) with VVC were ip treated with 3-IAld every day starting the day of infection and assessed for vaginal histology (Periodic Acid Shiff–staining of vaginal sections (scale bars, 100 μm) and PMN recruitment in the VF (mean % ± s.e.m., in the insets) at different dpi. Images were acquired using a microscope with a 40× objective and the analiSIS image processing software. Red arrows indicate fungi. AhR protein (D) and gene (E) expression by immunofluorescence staining of vaginal sections (Scale bars, 100 μm) and RT-PCR of vaginal tissues, respectively, in infected mice treated with 3-IAld. Images were acquired with a 40× objective and the analySIS image processing software. (F) Gene expression by RT-PCR at 3 (AhR and Cyp1a1) and 7 (Il18) dpi. *P < 0.05, **P < 0.01 and ***P < 0.001, ****P < 0.0001 treated vs. untreated (None) mice.