Figure 6. Beclin-1–deficient mice have a decreased profibrotic macrophage phenotype early in the disease process.

(A) Transmission electron microscopy (TEM) sections of the glomerular compartment after 2 months of cigarette smoke (CS) exposure compared with room air (RA), displaying normal podocyte foot processes in RA control (black arrowhead) and podocyte foot process effacement (black arrow) in CS mice, as well as mitochondrial swelling in CS-exposed mice. Scale bars: 500 nm (upper panels) and 1 μm (lower panels). (B) TEM sections of tubular compartment after 2 months of CS exposure compared with RA, displaying mitochondrial swelling in tubular cells in CS-exposed mice. Scale bars: 1 μm (upper panels) and 500 nm (lower panels). (C–E) Characterization of M1 or proinflammatory (Ly6c^hiF4/80⁺) and M2 or profibrotic (CD206⁺F4/80⁺) macrophages performed using flow cytometry, with evidence of (C) an increased Ly6C^hi iNOS-expressing population in Becn1^+/– compared with Becn1^+/+ mice (n = 10 for Becn1^+/+ RA, n = 12 for Becn1^+/+ CS, n = 7 for Becn1^+/– RA, n=9 for Becn1^+/+ CS), but (D and E) decreased infiltration of CD206⁺F4/80⁺ and Ly6C^lo populations in Becn1^+/– compared with Becn1^+/+ mice (n = 5 per group) after 2 months of CS exposure. All data are mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, analyzed by 1-way ANOVA with Bonferroni’s post hoc test.