Fig. 7. IL-9 promotes allergic inflammation by inducing CCL5 production from lung macrophages.

Arg1^fl/fl LysM-Cre^+/− mice were treated with HDM for 6 weeks.

(A), Arg1 expression in IMs was analyzed. BALF total cell number (B), BALF eosinophils (C), Lung eosinophils (D) and MLN cell number were analyzed (n = 4–10).

(F), UMAP showing Ccl5 expression from CITE-seq experiment described in Fig. 3.

(G), CCL5 expression in IMs was analyzed by flow cytometry (n = 4–10).

(H and I), Serum CCL5 level was analyzed by ELISA (n = 4–10).

(J), FACS sorted Arg1^+/− macrophages were treated with IL-9 for 24 hours, CCL5 level was measured by ELISA (n=3).

(K-L), Naïve mice were treated with IL-9 for three days, CCL5 and Arg1 expression from IMs were analyzed (n=4).

(M), CCL5 expression was analyzed by gating on Arg1⁺ or Arg1⁻ IMs from WT HDM treated mice (n=11).

(N), Human monocyte were cultured under M2 macrophage condition, CCL5 mRNA expression was analyzed (n = 3).

(O), IL-9 production from PBMCs was analyzed from non-asthma donors and asthma patients (n=7–9).

(P), Correlation between FEV1 corrected for height and IL-9 production from patient PBMCs.

(Q-R), Arginase activity (Q) and CCL5 level (R) was analyzed from non-asthma donors and asthma patients (n=5–9).

(S), Correlation of PBMC IL-9 and serum CCL5 concentration (n=11).

Data are presented as mean ± SEM from two independent experiments. Unpaired two-tailed Student t-test was used for comparison in B–C, D–E, H–I, K–L, N–O and Q–R. A paired two-tailed t-test was used to generate the p value in M. Two-way ANOVA with Sidak’s multiple comparisons was used for comparisons in J. Spearman correlation was performed for P and S, *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. See also Fig. S6.