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Does Hepatitis Affect The Liver

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Does Hepatitis Affect The Liver – Extracellular vesicles consist of lipid nanoparticles produced by different cell types of living organisms. They are known to carry proteins, metabolites, nucleic acids and lipids as cargo and are important mediators of cell-to-cell communication. A role for extracellular vesicles in chronic liver disease has been reported. Liver diseases such as viral hepatitis kill many people worldwide. Liver fibrosis has been associated with a type of viral hepatitis that causes liver disease in some patients, including cirrhosis, liver failure, and carcinoma. In this review, we discuss how extracellular vesicles can be used for communication between pathogens (hepatitis B and C viruses) and host cells, and how these complex cellular interactions may contribute to the development of chronic liver disease. We also discuss how understanding how these organisms work can help develop strategies to treat chronic liver disease.

Extracellular vesicles (EVs), described four decades ago (Chargaff and West, 1946; Wolf, 1967), are now recognized as important mediators of intercellular communication in chronic liver disease (CLD) (Ramakrishnaiah et al., 2013; Hirsova). et al., 2016; Devhare et al., 2017; Banales et al., 2019). These membrane-bound nanoparticles are released by various types of cells in living organisms and are known to carry cargo such as proteins, metabolites, nucleic acids, and lipids that mediate complex cellular communication. The peculiarity of cargo from electric vehicles has generated interest in the use of electric vehicles as a diagnostic tool and as a target for therapeutic treatment (Banales et al., 2019; Soekmadji et al., 2020).

Does Hepatitis Affect The Liver

CLD is an umbrella term used to describe any disease in which liver damage occurs over a period of 6 months or longer. CLD is a major public health problem worldwide; Hepatitis C, hepatitis B, alcoholic or nonalcoholic hepatitis, and autoimmune hepatitis are major causes of death and morbidity worldwide. An estimated 844 million people are living with CLD (2017) and there are at least 2 million CLD-related deaths per year worldwide (Byass, 2014). Cellular interactions between cell types such as hepatic progenitor cells (LPCs), hepatic stellate cells (HSCs) and Kupffer cells are implicated in the development of liver fibrosis and CLD, which eventually progress to end-stage liver disease, including cirrhosis. , liver failure and carcinoma (Dwyer et al., 2014; Pozniak et al., 2017). Recently, EVs have been shown to interact with these complex cells among liver cell types, particularly in CLD, highlighting their potential role in disease development (Deng et al., 2017).

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This review discusses the role that EVs can play in mediating communication between pathogens and host cells and how EV-mediated cell-cell interactions contribute to the development of liver disease. We also discuss how understanding how these organisms work can help develop strategies to treat chronic liver disease.

The liver is the largest organ in the body, accounting for approximately 2–5% of the body weight of an adult, with approximately 10% of the body’s blood circulating at any given time (Vekemans and Braet, 2005). The liver performs many homeostatic functions related to metabolism, digestion, immunity, and the endocrine system. The liver consists of two main types of cells, parenchymal and non-parenchymal cells (Trefts et al., 2017). Parenchymal cells, including hepatocytes and cholangiocytes, make up most of the cell types in the liver. Hepatocytes, along with hepatic sinusoidal endothelial cells (LSEC), line the sinusoids and are the primary epithelial cells of the liver (Trefts et al., 2017). Hepatocytes and LSECs are separated by a perisinusoidal space, also known as the space of Dissé. Cholangiocytes line the bile duct and are involved in the production and transformation of bile (Figure 1).

Figure 1 Schematic representation of the liver and one end of the lobe. The portal triad formed by the hepatic artery, bile duct and portal vein is located at both ends of the liver lobe. Blood collected from the portal vein and hepatic vein flows directly to the central vein through the hepatic sinusoids, which contain hepatic sinusoidal endothelial cells (LSEC) and hepatocytes. Hepatocytes and LSEC are separated by a perisinusoidal space, also known as the space of Dissé, where hepatic stellate cells (HSCs) reside. Hepatocytes secrete bile, which flows into bile ducts formed by cholangiocytes. The duct of Herring is located at the junction between cholangiocytes and hepatocytes, where liver progenitor cells (LPCs) are supposed to originate.

In the injured liver, a special subset of stem cells called hepatic or hepatic progenitor cells (LPCs), also called circulating cells in rats, can regenerate the liver by differentiating into hepatocytes or cholangiocytes (Tirnitz-Parker et al., 2010; Köhn-Gaone et al., 2016 ). LPCs are thought to originate in small numbers from the canal of Hering in a stable environment, but rapidly proliferate after liver injury (Dwyer et al., 2014). Although their origin is still debated, recent lineage tracing studies have shown that they originate from Sox9

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Ductal cells proliferate and differentiate into human progenitor cells (LPCs) after chronic insult (Furuyama et al., 2011).

The non-parenchymal cells of the liver consist of hepatic myofibroblast cells called hepatic stellate cells (HSCs), liver-resident macrophages or Kupffer cells, and LSECs. HSCs, normally located in the perisinusoidal space, are liver mesenchymal cells that contain vitamin A (Higashi et al., 2017). They are found in the human liver at a ratio of 3.6 to 6 cells per 100 hepatocytes, and their main function in the normal liver appears to involve the storage of vitamin A (Moreira, 2007). Studies have also reported their role in the regulation of blood pressure and venous pressure at steady state (Geerts, 2001). LSECs are specialized endothelial cells that form the sinusoidal endothelium, which is important for the exchange of water, nutrients, and solvents between sinusoidal blood and hepatocytes (Ni et al., 2017). They are highly endocytic and have a well-developed clathrin-mediated endocytosis mechanism (Simon-Santamaria et al., 2010). Finally, Kupffer cells are liver-specific macrophages. They form part of the reticuloendothelial system and are involved in the removal of senescent cells and pathogens such as bacteria and viruses. They are one of the most important guarantors of liver protection.

Although the liver is a highly regenerative organ, long-term insults from pathogens, metabolic insults, and other toxic agents can lead to the development of CLD, where the liver’s ability to repair and regenerate is reduced due to liver damage (fibrosis). ). ) and eventually lead to liver damage. The development of CLD is a complex process involving different cell types. After liver damage, the liver attempts to repair the damaged tissue through the normal healing process. Paracrine stimulatory signals, including inflammatory mediators from other cell types such as LPCs, LSECs, Kupffer cells, and hepatocytes in the liver microenvironment, activate dormant HSCs leading to proliferation and migration to the primary insult site. These activated α-smooth muscle actin (SMA) and collagen type I-expressing HSCs transdifferentiate into myofibroblasts, which produce collagen and extracellular matrix necessary for wound healing (Higashi et al., 2017). They rapidly lose their ability to store vitamin A, leading to a decrease in intracellular vitamin A levels as they divide and divide the vitamin A lipid droplets into two daughter cells (Higashi et al., 2005). In CLD, these HSC-derived myofibroblasts contribute to the deposition of collagen and extracellular matrix due to liver injury; thus responsible for liver fibrosis in a variety of CLDs in adults, including hepatitis C virus (HCV), alcoholic liver disease, non-alcoholic liver disease (Friedman, 2008), liver cancer (Bridle et al., 2001), hemochromatosis (Ramm et al., 1997), as well as pediatric liver diseases such as biliary atresia (Ramm et al., 1998) and cystic fibrosis (Lewindon et al., 2002).

LPCs can rapidly proliferate and differentiate in response to liver injury in a process known as the ductular reaction. However, the role of LPC in liver regeneration and repair appears to be limited to transient injuries where replication of mature hepatocytes is impaired or the liver microenvironment is significantly altered (Dollé et al., 2010; Best et al., 2013). ). Clouston et al. showed that inflammatory cytokines such as interferon (IFN)-γ inhibit hepatocyte proliferation, resulting in LPC proliferation (Clouston et al., 2005). One possible mechanism of LPC development involves tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 (Fn14) signaling (TWEAK/Fn14 signaling) (Dwyer et al., 2014). Binding of TWEAK released by macrophages or natural killer (NK) cells to Fn14 expressed on the surface of LPCs activates the downstream NFkB signaling pathway, which transactivates genes involved in proliferation, leading to LPC proliferation (Tirnitz-Parker et al., 2010; Viebahn et al. , 2010; Bird et al., 2013).

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Interactions between HSCs and LPCs have been shown to induce liver fibrogenesis in CLD. Notch signaling was associated with Notch1/Notch2 expression

Myofibroblasts (Boulter et al., 2012). This study showed a decrease in biliary gene expression in LPCs when a Notch inhibitor was used under confluent conditions.

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