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. 2015 Feb 20;11(1):166–182. doi: 10.4161/15548627.2014.981915

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Majid Sakhi Jabir, Lee Hopkins, Neil D. Ritchie, Ihsan Ullah, Hannah K. Bayes, Dong Li, Panagiotis Tourlomousis, Alison Lupton, Daniel Puleston, Anna Katharina Simon, Clare Bryant, and Thomas J. Evans

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — Autophagy downregulates activation of the inflammasome by P. aeruginosa. (A) BMDMs from wild-type mice (Vav1-atg7^+/+) or mice with a conditional deletion of Atg7 in bone marrow-derived cells (Vav1-atg7^−/−) were infected with PA103ΔUΔT and autophagy quantified. Panels show immunoblots for indicated proteins in cells infected as shown. Graphs show secretion of active IL1B and TNF from basal and infected BMDMs as shown. Columns are means of 3 independent determinations; error bars are SEM. * indicates a significant difference between the levels in BMDMs from WT or Vav1-atg7^−/− mice, P < 0.05. n.s., not significant. (B) As (A), but in cells depleted of Atg5 by siRNA knockdown as shown. (C) As (A) but in cells depleted of Lc3b by siRNA knockdown as shown and infected as indicated. ** indicates a significant difference between the levels in BMDMs from Lc3b siRNA-treated cells and control, P < 0.01. ((D)to F) Immunoblots of key proteins (including the ATG12&z.vrecto;ATG5 conjugate) of (A) to (C) depleted by knockout or knockdown as shown, with TUBB5/β-tubulin as control. C is control. D, BMDMs from WT or Vav1-atg7 knockout animals as shown probed for ATG7. (E) and (F), BMDMs treated with siRNA or control siRNA to Atg5 (E) and Lc3b (F).