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

Bijnen, Mitchell; Josefs, Tatjana; Cuijpers, Ilona; Maalsen, Constantijn J; Gaar, José van de; Vroomen, M.; Wijnands, Erwin; Rensen, Sander S.; Greve, Jan; Hofker, Marten H.; Biessen, Erik A. L.; Stehouwer, Coen D. A.; Schalkwijk, Casper G.; Wouters, Kristiaan

doi:10.1136/gutjnl-2016-313654

Cited by 106 publications

(86 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ATMs especially release a high amount of neutrophil chemotactic proteins that increase neutrophil recruitment liver and worsen liver injury 42 . Indeed, clinical studies reported a significant correlation of ATMs with neutrophil and macrophage content in liver biopsies 43 as well as with steatosis severity and fibrosis indexes 44 . The crosstalk between liver and adipose tissue also involves the adipocytokines.…”

Section: Fatty Liver Disease: Crosstalk With Surrounding Tissuesmentioning

confidence: 99%

Macrophages in the pathophysiology of NAFLD: The role of sex differences

Ministrini

Montecucco

Sahebkar

et al. 2020

Eur J Clin Investigation

View full text Add to dashboard Cite

Nonalcoholic fatty liver disease (NAFLD) is a multifactorial pathological condition, which recognizes a certain sexual dimorphism. Experimental and clinical studies provided evidence for a critical role of macrophages in NAFLD development and progression. Especially, liver-resident macrophages (also known as Kupffer cells) are likely the common final pathway of several pro-steatosic signals. A huge amount of danger-associated molecular patterns recognized by Kupffer cells is provided within the liver by lipid and glucose toxicity. Other pro-inflammatory signals come from surrounding tissues into the portal vein, directly to the liver: they come from dysfunctional adipocytes, adipose tissue macrophages and gut dysbiosis. These complex crosstalks are differently represented across sexes, as sexual hormones control many of these processes. Sexual dimorphism then modulates metabolic and inflammatory cascades driving the liver from a simple steatosis to NAFLD and beyond.Here, metabolic and inflammatory mechanisms underlying NALFD pathophysiology will be updated. A special attention will be paid to describe sex-related differences that could provide insights for patient stratification and more tailored therapeutic approaches. K E Y W O R D Sinflammation, Kupffer cells, macrophages, microbiome, nonalcoholic fatty live disease 2 of 9 | MINISTRINI eT al.

show abstract

Section: Fatty Liver Disease: Crosstalk With Surrounding Tissuesmentioning

confidence: 99%

Macrophages in the pathophysiology of NAFLD: The role of sex differences

Ministrini

Montecucco

Sahebkar

et al. 2020

Eur J Clin Investigation

View full text Add to dashboard Cite

show abstract

“…As mentioned previously, impaired suppression of insulin-mediated lipolysis in white adipose tissue (WAT) leads to hepatic steatosis through increased fatty acid uptake of hepatocytes (Figure 1). In addition, inflammation in WAT systemically affects hepatic inflammation (74). Lean mice transplanted with visceral adipose tissue from obese mice exhibited elevated infiltration of neutrophils and macrophages in the liver and ultimately suffered from aggravated liver damage after NASH diet feeding (74).…”

Section: “Multiple-parallel Hit” Pathogenesis Of Nashmentioning

confidence: 99%

“…In addition, inflammation in WAT systemically affects hepatic inflammation (74). Lean mice transplanted with visceral adipose tissue from obese mice exhibited elevated infiltration of neutrophils and macrophages in the liver and ultimately suffered from aggravated liver damage after NASH diet feeding (74). However, transplantation of visceral fat from obese mice with depletion of adipose tissue macrophage (ATM) by treatment with clodronate liposomes did not cause hepatic inflammation in lean mice (74), suggesting that ATM directly contributes to hepatic inflammation and NASH progression.…”

Section: “Multiple-parallel Hit” Pathogenesis Of Nashmentioning

confidence: 99%

“…Lean mice transplanted with visceral adipose tissue from obese mice exhibited elevated infiltration of neutrophils and macrophages in the liver and ultimately suffered from aggravated liver damage after NASH diet feeding (74). However, transplantation of visceral fat from obese mice with depletion of adipose tissue macrophage (ATM) by treatment with clodronate liposomes did not cause hepatic inflammation in lean mice (74), suggesting that ATM directly contributes to hepatic inflammation and NASH progression. Furthermore, adipokines (such as adiponectin and leptin) secreted from WAT have reported to affect lipid accumulation, inflammation, and fibrosis in the liver (Figure 1) (75).…”

Section: “Multiple-parallel Hit” Pathogenesis Of Nashmentioning

confidence: 99%

See 1 more Smart Citation

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

Kim

Lee

2018

Front. Endocrinol.

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is an emerging global health problem and a potential risk factor for type 2 diabetes, cardiovascular disease, and chronic kidney disease. Nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, is a predisposing factor for development of cirrhosis and hepatocellular carcinoma. The increasing prevalence of NASH emphasizes the need for novel therapeutic approaches. Although therapeutic drugs against NASH are not yet available, fundamental insights into the pathogenesis of NASH have been made during the past few decades. Multiple therapeutic strategies have been developed and are currently being explored in clinical trials or preclinical testing. The pathogenesis of NASH involves multiple intracellular/extracellular events in various cell types in the liver or crosstalk events between the liver and other organs. Here, we review current findings and knowledge regarding the pathogenesis of NASH, focusing on the most recent advances. We also highlight hormone-based therapeutic approaches for treatment of NASH.

show abstract

“…Bijnen et al 2 expand on the role of AT inflammation and its effects on NAFLD, investigating how AT inflammation contributes to immune cell recruitment to the liver. The first indication that inflammatory CD11c + ATMs impacted on liver immune cell populations came by identifying a positive correlation between the abundance of CD11c + ATMs and liver macrophages in obese mice.…”

mentioning

confidence: 99%

Take me to the liver: adipose tissue macrophages coordinate hepatic neutrophil recruitment

Pernes

Lancaster

Murphy

2018

Gut

View full text Add to dashboard Cite

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

Abstract: ATMs from obese vAT induce hepatic macrophage accumulation during NASH development, possibly by enhancing neutrophil recruitment.

Cited by 106 publications

References 37 publications

Macrophages in the pathophysiology of NAFLD: The role of sex differences

Macrophages in the pathophysiology of NAFLD: The role of sex differences

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

Take me to the liver: adipose tissue macrophages coordinate hepatic neutrophil recruitment

Contact Info

Product

Resources

About