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In vitro research found that metformin activated a novel galectin-directed ubiquitin signal transduction system in response to lysosomal membrane damage, induces autophagy, and facilitates the elimination of M.tb from macrophages [117]

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The current consensus is that macrophages recruited into the gut in IBD have a greater pro-inflammatory potential than resident macrophages, and this would support the notion that increased sensitivity of the recruited cells to pro-death signals could limit inflammation, while the opposite could be envisaged for resident macrophages