Potential role of hepatic macrophages in neutrophil-mediated liver injury in rats with sepsis

Hepatology ◽  
1993 ◽  
Vol 17 (6) ◽  
pp. 1086-1094 ◽  
Author(s):  
Fukashi Doi ◽  
Tomomochi Goya ◽  
Motomichi Torisu
Keyword(s):  
Liver Injury ◽  
Potential Role ◽  
Hepatic Macrophages

scholarly journals Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

2021 ◽  
Vol 22 (14) ◽  
pp. 7249
Author(s):  
Siyer Roohani ◽  
Frank Tacke
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Current Knowledge ◽  
Hepatocellular Cancer ◽  
Complete Recovery ◽  
Hepatic Macrophages ◽  
Liver Injuries ◽  
Microbial Products ◽  
Injured Liver

The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

Potential role of catalase in mice with lipopolysaccharide/D-galactosamine-induced fulminant liver injury

2013 ◽  
Vol 44 (11) ◽  
pp. 1151-1158 ◽  
Author(s):  
Mengying Jia ◽  
Yuping Jing ◽  
Qing Ai ◽  
Rong Jiang ◽  
Jingyuan Wan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Potential Role

scholarly journals Assessment of the Potential Role of Silymarin Alone or in Combination with Vitamin E and/ or Curcumin on the Carbon Tetrachloride Induced Liver Injury in Rat

2015 ◽  
Vol 58 (6) ◽  
pp. 833-842 ◽  
Author(s):  
Nouf Al-Rasheed ◽  
Laila Faddah ◽  
Iman A Sharaf ◽  
Azza M Mohamed ◽  
Nawal Al-Rasheed ◽  
...  
Keyword(s):  
Vitamin E ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Potential Role

scholarly journals Caveolin-1 Deficiency Protects Mice Against Carbon Tetrachloride-Induced Acute Liver Injury Through Regulating Polarization of Hepatic Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Ziheng Yang ◽  
Jie Zhang ◽  
Yan Wang ◽  
Jing Lu ◽  
Quan Sun
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Liver Diseases ◽  
Acute Liver Injury ◽  
Mrna Levels ◽  
Alcoholic Fatty Liver ◽  
Caveolin 1 ◽  
Hepatic Macrophages ◽  
M1 Phenotype

Polarization of hepatic macrophages plays a crucial role in the injury and repair processes of acute and chronic liver diseases. However, the underlying molecular mechanisms remain elusive. Caveolin-1 (Cav1) is the structural protein of caveolae, the invaginations of the plasma membrane. It has distinct functions in regulating hepatitis, cirrhosis, and hepatocarcinogenesis. Given the increasing number of cases of liver cancer, nonalcoholic steatohepatitis, and non-alcoholic fatty liver disease worldwide, investigations on the role of Cav1 in liver diseases are warranted. In this study, we aimed to investigate the role of Cav1 in the pathogenesis of acute liver injury. Wild-type (WT) and Cav1 knockout (KO) mice (Cav1tm1Mls) were injected with carbon tetrachloride (CCl4). Cav1 KO mice showed significantly reduced degeneration, necrosis, and apoptosis of hepatocytes and decreased level of alanine transaminase (ALT) compared to WT mice. Moreover, Cav1 was required for the recruitment of hepatic macrophages. The analysis of the mRNA levels of CD86, tumor necrosis factor (TNF), and interleukin (IL)-6, as well as the protein expression of inducible nitric oxide synthase (iNOS), indicated that Cav1 deficiency inhibited the polarization of hepatic macrophages towards the M1 phenotype in the injured liver. Consistent with in vivo results, the expressions of CD86, TNF, IL-6, and iNOS were significantly downregulated in Cav1 KO macrophages. Also, fluorescence-activated cell sorting (FACS) analysis showed that the proportion of M1 macrophages was significantly decreased in the liver tissues obtained from Cav1 KO mice following CCl4 treatment. In summary, our results showed that Cav1 deficiency protected mice against CCl4-induced acute liver injury by regulating polarization of hepatic macrophages. We provided direct genetic evidence that Cav1 expressed in hepatic macrophages contributed to the pathogenesis of acute liver injury by regulating the polarization of hepatic macrophages towards the M1 phenotype. These findings suggest that Cav1 expressed in macrophages may represent a potential therapeutic target for acute liver injury.

scholarly journals An experimental study to identify the potential role of pharmacogenomics in determining the occurrence of oxaliplatin‐induced liver injury

HPB ◽  
2013 ◽  
Vol 15 (8) ◽  
pp. 581-587 ◽  
Author(s):  
Stuart M. Robinson ◽  
Jelena Mann ◽  
Derek M. Manas ◽  
Derek A. Mann ◽  
Steven A. White
Keyword(s):  
Experimental Study ◽  
Liver Injury ◽  
Potential Role

First Experience on Bilirubin Removal with a Hemoadsorption Column (Lixelle®) in a Child with Cardiogenic Liver Injury

2017 ◽  
Vol 40 (9) ◽  
pp. 522-525 ◽  
Author(s):  
Gabriella Bottari ◽  
Andrea Moscatelli ◽  
Enrico E. Verrina ◽  
Franco Lerzo ◽  
Fabio S. Taccone
Keyword(s):  
Liver Injury ◽  
Potential Role ◽  
C Reactive Protein ◽  
Progressive Reduction ◽  
Reactive Protein ◽  
Persistent Inflammation ◽  
First Case ◽  
Congestive Liver ◽  
Severe Hyperbilirubinemia

Introduction Hyperbilirubinemia may have deleterious effects on many organs, even after the neonatal age. Blood purification is effective in the treatment of hyperbilirubinemia. Recently some reports suggest the potential role of hemoadsorption columns in this setting. Methods We present the case of a 6-year-old child with severe hyperbilirubinemia due to congestive liver dysfunction, complicated by persistent inflammation, immunosuppression and catabolism syndrome (PICS). The patient was treated with a hemoadsorption column (Lixelle®) in combination with continuous veno-venous hemodiafiltration (CVVHDF). Results During treatment, a significant and rapid decrease in total bilirubin (TB) and other indices of cholestasis was observed. Furthermore, a progressive reduction in the inflammatory biomarkers (Procalcitonin, C-reactive protein) occurred. These results persisted at the discontinuation of therapy. Conclusions To our knowledge this is the first case in which hemoadsorption with the Lixelle® adsorbing column in combination with CVVHDF has been used to manage pediatric hyperbiliribinemia secondary to cardiogenic liver injury.

POPDC proteins and cardiac function

2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand
Keyword(s):  
Potential Role ◽  
Striated Muscle ◽  
Short Review ◽  
Effector Proteins ◽  
Muscle Disease ◽  
Disease Genes ◽  
Protein Protein Interaction ◽  
Interaction Partners ◽  
And Function

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.

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