Mo-MMs recruited by enteric neurons via the CCL2 axis facilitate myenteric plexus remodeling. (A) Complementary to Fig. 5, F and G: confocal images of colonic myenteric plexus from tamoxifen- and 3×DSS- or water-treated SLICK-H^ER-CreCcl2^fl/fl (Cre⁺) and Ccl2^fl/fl (Cre^–) littermates, stained with antibodies specific to MHCII (MMs), Hu (neuronal somas), and βIII-tubulin (nerve fibers). Images are representative of control and DSS mice (DSS Cre^– and Cre⁺, n = 7–8 per group; water Cre^– baseline, n = 4–6). Scale bars, 100 μm. (B) Complementary to Fig. 5 G: structural changes in colonic myenteric plexus of mice described in A quantified by confocal microscopy, showing counts of neuron clusters, counts of Hu⁺ neurons per cluster, and counts and area of IGFT regions (DSS Cre^– and Cre⁺, n = 7–8; water Cre^– baseline, n = 4–6). Each value is the mean per mouse. P values above each column show statistical differences against baseline. (C) Complementary to Fig. 5 I: confocal images of colonic myenteric plexus from mice described in A at week 1, stained with CC7 (apoptotic cells) and ANNA-1 (neuronal somas) antibodies. Images are representative of control and DSS mice (DSS Cre^– and Cre⁺, n = 4 per group; water Cre^– baseline, n = 2). White arrowheads point to clusters of CC7⁺ANNA-1⁺ neurons. Scale bars, 100 μm. Graphs show the mean ± SEM, n—mouse. Data are representative of at least two independent experiments with similar results. Statistical analyses: two-way ANOVA for multiple comparisons (B), *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, and ****P ≤ 0.0001.