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Inflammation is increasingly recognised to critically determine the clinical course and outcome of acute liver failure (ALF). On the one hand, massive hepatocyte cell death triggers immune cell activation and recruitment to the liver, which can stimulate immune-mediated liver damage. On the other hand, systemic activation of inflammation, systemic inflammatory response syndrome, promotes multiple organ failure and defective antimicrobial responses.1 Innate immune mechanisms play a prominent role in ALF. Mouse models of acute liver injury revealed that liver-resident macrophages, Kupffer cells, sense hepatocyte-mediated release of alarmins, which results in Kupffer cell activation and cytokine release.2 Hence, neutrophils and monocytes are recruited from the bloodstream to the site of injury. During the early phase after recruitment, neutrophils and monocytes have an inflammatory phenotype and aggravate tissue damage.3 4 However, there is ample experimental evidence that monocyte-derived macrophages change their phenotype in the liver, if injury has terminated, towards repair-promoting phagocytes.5 6 Up to now, the ‘human counterpart’ of inflammatory versus restorative macrophages in ALF has been vague. In this issue of Gut, Dr. Antoniades and coworkers present compelling experimental evidence from human samples and a mouse model that restorative macrophages in ALF …
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