Kuffer cells

Federal government websites often end in. The site is secure. Kupffer cells are resident kuffer cells macrophages and play a critical role in maintaining liver functions.

AoH publishes editorials, opinions, concise reviews, original articles, brief reports, letters to the editor, news from affiliated associations, clinical practice guidelines and summaries of congresses in the field of Hepatology. Our journal seeks to publish articles on basic clinical care and translational research focused on preventing rather than treating the complications of end-stage liver disease. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact.

Kuffer cells

Aims: Kupffer cells KCs are the liver-resident macrophages and play a leading role in the regulation of liver homeostasis in physiological conditions and in pathology. The study aims to investigate the anti-echinococcosis effect of KCs and the effects of hepatic stellate cells HSCs activation in the progression of liver fibrosis in hepatic alveolar echinococcosis hepatic AE. It is worth noticing that the expression levels of anti-inflammatory cytokines were slightly higher than that of pro-inflammatory cytokines. Conclusions: Our research indicates that KCs have immune-protective effect of anti-echinococcosis and promote liver fiber repair, and it also suggests that they have potential therapeutic value for patients with hepatic AE. Alveolar echinococcosis AE , caused by Echinococcus multilocularis. As most cases involve the liver, patients may suffer from hepatomegaly and recurrent jaundice Menghi et al. Cysts localize first in the liver, and in the early stages, the infection is generally asymptomatic Arrechea Irigoyen et al. As the growth pattern of the cyst is similar to a malignant tumor, the WHO has proposed that a clinical classification that is similar to TNM Tumor, Node, Metastases classification of tumors. Such classification is a necessary tool when making therapeutic decisions for the treatment of this disease Kern et al. AE is a serious life-threatening chronic helminthiasis caused by E. It mostly occurs in the liver and is known to be slowly progressive but often, a fatal disease. It is estimated that nearly 2 billion people worldwide are infected with worms Hotez et al. Some experimental studies, including experimental studies on infected mice and immunological studies on AE patients, have revealed that complex host-parasite interaction occurs in the process of E. The variability and severity of the clinical manifestations of this parasitic disease are related to the duration and degree of infection Mezioug and Touil-Boukoffa, Liver fibrosis is one of the main pathological changes in the progression of hepatic AE.

Whereas late KC depletion after day 14 has a completely inverse effect: it decreased tumor growth. Taken together, these findings show kuffer cells macrophages, specifically KCs, are required for BG-induced anti-metastatic activity in the liver. Friedman SL.

Federal government websites often end in. The site is secure. Kupffer cells are a critical component of the mononuclear phagocytic system and are central to both the hepatic and systemic response to pathogens. Kupffer cells are reemerging as critical mediators of both liver injury and repair. Multiple M2 phenotypes can be distinguished, each involved in the resolution of inflammation and wound healing. Here, we have provided an update on recent research that has contributed to the developing delineation of the contribution of Kupffer cells to different types of liver injury, with an emphasis on alcoholic and nonalcoholic liver diseases. These recent advances in our understanding of Kupffer cell function and regulation will likely provide new insights into the potential for therapeutic manipulation of Kupffer cells to promote the resolution of inflammation and enhance wound healing in liver disease.

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Tissue macrophages are highly adapted to their tissue of residence, but it is unclear how they become specialized from common progenitors. Now, complementary studies from the Guilliams and Glass laboratories detail many of the precise cellular and molecular interactions that promote Kupffer cell KC specialization in the liver. Imaging studies by Bonnardel et al. One population had arrested, showed a KC-like morphology and acquired KC-associated transcription factors; the other monocytes remained small, round and motile. Arrested monocytes were visualized extending processes across the endothelium and contacting hepatic stellate cells, which are pericytes found in the perisinusoidal space of Disse. Although KCs are thought to strictly reside within sinusoidal blood vessels, the authors found that steady state KCs also closely associated with stellate cells.

Kuffer cells

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Liver macrophages comprise Kupffer cells — which are self-maintaining, non-migratory tissue-resident phagocytes that originate from yolk sac-derived precursors during embryogenesis — and monocyte-derived macrophages. Kupffer cells are essential for hepatic and systemic homeostasis, as they contribute to metabolism, scavenge bacteria and cellular debris, and induce immunological tolerance.

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Transcriptomic and epigenetic mechanisms underlying myeloid diversity in the lung. CA: A Cancer J. Moreover they up-regulate antigen presentation and recruit TH2 T helper cells type 2 responses [ 52 , 53 ]. Toll-like receptors as targets in chronic liver diseases. Mechanisms of hepatic fibrogenesis. Padovan, E. This tolerogenic property of KCs is essential to prevent undesired immune responses under the physiological conditions. Pathol Int. A possible reason for this could be due to the liver tissue already being at the anti-inflammatory and self-repairing stage, when the patients with hepatic AE received surgery. Here, we will first review the deleterious role of Kupffer cells in metabolic liver diseases and then summarize data demonstrating that Kupffer cells are protective in other types of liver injury, such as drug-induced liver injury and fibrosis. The development of steatosis, inflammation, fibrosis, and cirrhosis is a complex process involving both parenchymal and nonparenchymal cells resident in the liver, as well as the recruitment of other cell types to the liver in response to damage and inflammation Download PDF Bibliography. Hepatology, 50 , pp. Muramyldipeptide and diaminopimelic acid-containing desmuramylpeptides in combination with chemically synthesized Toll-like receptor agonists synergistically induced production of interleukin-8 in a NOD2- and NOD1-dependent manner, respectively, in human monocytic cells in culture. Thurman RG.

Federal government websites often end in. The site is secure. Chronic alcohol consumption is linked to the development of alcohol-associated liver disease ALD.

Biochem Soc Symp. Hepatitis C virus-induced CCL5 secretion from macrophages activates hepatic stellate cells. Federal government websites often end in. Cancer 4 , 1—10 Atorvastatin protects obese mice against hepatic ischemia-reperfusion injury by Toll-like receptor-4 suppression and endothelial nitric oxide synthase activation. However, myeloid depletion strategies are susceptible to the emergence of compensatory myeloid responses that paradoxically support tumor outgrowth EBioMedicine 53 , Hepatology 58, — Since transcriptional profiling revealed that KCs respond to BG via upregulation of genes associated with antigen presentation and interferon response Fig. Our study firstly performed pathological scoring on liver lesions of patients with hepatic AE, including common items such as inflammatory cell infiltration, cholestasis etc. Recent gene array studies of expression of candidate genes in the livers of patients with alcoholic hepatitis found that several components of the NADPH oxidase complex were upregulated, including rac-1, p22 phox , and gp91 phox