Figure 7.

Genetic ablation of vascular autophagy (canonical and non-canonical) promotes exaggerated and more rapid leukocyte trafficking

(A and B) Chimeric Atg5^fl/fl and Atg5^ΔEC mice were subjected to (A) LPS-induced peritonitis (n = 6–12 mice/group) or (B) skin inflammation (n = 5–6 mice/group), and neutrophil infiltration was quantified by flow cytometry or myeloperoxidase (MPO) activity, respectively.

(C) Atg5^fl/fl and Atg5^iΔEC mice were subjected to LPS-induced peritonitis, and neutrophil infiltration was quantified by flow cytometry (n = 4–9 mice/group).

(D) WT and Atg16L1^E230 mice were subjected to MDP-induced peritonitis, and neutrophil infiltration was quantified by flow cytometry (n = 4–5 mice/group).

(E and F) Non-chimeric (E) and (F) chimeric WT and Atg16L1^E230 mice were subjected to local IR injury, and neutrophil extravasation was assessed by confocal microscopy (n = 6–8 mice/group).

(G–I) Chimeric Atg5^fl/fl and Atg5^ΔEC mice were subjected to zymosan-induced peritonitis, and infiltration of (G) neutrophils, (H) monocytes, and (I) eosinophils at the indicated times was quantified by flow cytometry (n = 3–9 mice/group).

Means ± SEMs. Statistically significant difference from controls or between indicated groups is shown by ^∗p < 0.05, ^∗∗p < 0.01, and ^∗∗∗p < 0.001.