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. Author manuscript; available in PMC: 2024 Jan 2.
Published in final edited form as: Sci Signal. 2023 Sep 12;16(802):eabc9089. doi: 10.1126/scisignal.abc9089

Fig. 7. Fluoxetine diminishes HDM-induced lung inflammation and airway hyperresponsiveness.

Fig. 7.

(A) Mice were sensitized and challenged with HDM while receiving fluoxetine or PBS treatments. Animals and tissue were analyzed on day 23. (B) Methacholine-induced lung resistance was measured in anesthetized mice using a Scrieq flexivent instrument. Data are pooled from 2 independent experiments with N=8/group total. (C) Digested lung tissue single cell suspension was analyzed by flow cytometry for mast cells (FcεRI+cKit+), eosinophils (siglecF+CCR3hi) and Th2 cells (CD3+CD4+IL13+IL4+). N=11–14/group. (D) BALF cells were analyzed for T cells (CD90.2+/MHC II-neg), B cells (B220+MHCII+), eosinophils (SiglecF+CCR3+) and neutrophils (CD11b+Ly6G+). Data are pooled from at least 2 independent repeats with each point representing an individual mouse. N=9/group. (E) BALF cytokines were measured by ELISA. Data are pooled from 3 independent experiments. N=10–18/group. (F) Plasma MCPT-1 levels were measured by ELISA from two independent experiments. N=8/group. (G) Lung sections were stained for mucus production with PAS (left) or H&E (right) and blinded samples were scored as described in Materials and Methods. Data are pooled from 2 independent experiments. N=9/group. (H) Anti-HDM IgG and total IgE in plasma were determined by ELISA from two independent experiments. N=11–15/group. All replicates are biological. Statistical values were determined by 1-way ANOVA (Tukey’s test) *p<.05; **p<.001; ****p<.0001 N.D.=not detected.