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. Author manuscript; available in PMC: 2022 Nov 15.
Published in final edited form as: Immunity. 2021 Sep 9;54(11):2595–2610.e7. doi: 10.1016/j.immuni.2021.08.009

Figure 1. Candidalysin is necessary for the induction of allergic airway disease in mice.

Figure 1.

(A) C57BL/6 mice were challenged intranasally with 105 viable cells of wildtype parental strain or ece1Δ/Δ C. albicans as indicated in the timeline.

(B) Respiratory system resistance (RRS) was assessed after intravenous injection of increasing doses of acetylcholine (Ach). (C) Quantitation of cells from bronchoalveolar lavage fluid samples (mac, macrophages; eos, eosinophils; neu, neutrophils; lym, lymphocytes).

(D) Cytokines quantitated by ELISA from deaggregated lung supernatants.

(E and F) T cells from lungs analyzed by flow cytometry. (E) Representative flow plot of TH1 (T-bet positive), Th2 (GATA3 positive), and Th17 (RORγt positive) cells from lungs after challenge. (F) Aggregate T cell data expressed as percentages and absolute cell numbers.

(G) C. albicans colony-forming units (CFU) cultured from lungs.

(H) Hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining of 5 mm lung sections from mice challenged under the indicated conditions.

n ≥ 4, mean ± SEM. n.s., not significant; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, using two-tailed Student’s t test (F) or one-way ANOVA followed by Tukey’s test (A–D and G) for multiple comparison. Magnification: 40× and 200×. Scale bars, 500 or 50 μm, respectively. Data are representative of three independent experiments. See also Figures S1 and S2.