Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice

Abstract

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Adipose tissue remodelling in obese subjects is a determinant of presence and severity of fatty liver disease

“…In obesity, an increased number of activated macrophages in the VAT lead to local chronic inflammation and VAT dysfunction 36,42,43 . Bijnen et al 44 showed that the transplantation of macrophage infiltrated VAT from obese to lean mice was able to induce macrophage recruitment into the liver and NASH development, underlining the role of these cells in the cross‐talk between liver and VAT 44 . Thus, in order to perform an accurate description of phenomena associated with VAT impairment, which could lead to hepatic and extrahepatic metabolic complications of obesity, we measured VAT levels of both netrin‐1 and UNC5B, which is a netrin‐1‐dependent macrophage retention factor secreted in condition of fatty acids accumulation 45 .…”

Multiple Parallel Hits Hypothesis in Nonalcoholic Fatty Liver Disease: Revisited After a Decade

“…Bijnen and colleagues transplanted VAT from lean, obese, or ATM‐depleted obese mice to lean Ldr −/− mice. ( 38 ) AT transplantation from obese mice resulted in increased liver injury and hepatic inflammation, which was less pronounced in ATM‐depleted transplanted AT. Liver injury was paralleled by increased numbers of circulating and hepatic neutrophils, an effect mainly attributed to increased synthesis of the neutrophil chemotaxis proteins chemokine (C‐X‐C motif) ligands 14 and 16 by ATM.…”

“…Liver injury was paralleled by increased numbers of circulating and hepatic neutrophils, an effect mainly attributed to increased synthesis of the neutrophil chemotaxis proteins chemokine (C‐X‐C motif) ligands 14 and 16 by ATM. ( 38 )…”

A Novel Subset of CD95+ Pro-Inflammatory Macrophages Overcome miR155 Deficiency and May Serve as a Switch From Metabolically Healthy Obesity to Metabolically Unhealthy Obesity

“…Seminal studies of obesity have helped us to understand that macrophages secrete TNFα, which further enhances lipolysis, thereby driving metabolic dysfunction ( 61 ). Moreover, when this occurs in the visceral adipose tissue (VAT), collateral damage to nearby organs, such as liver and pancreas, can lead to metabolic dysfunction of these organs ( 62 , 63 ). Regarding the mechanism of MHO, a previous report showed that TNFα can increase Fas expression ( 64 ).…”