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      Increased Liver Localization of Lipopolysaccharides in Human and Experimental NAFLD

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          Abstract

          Lipopolysaccharides (LPS) is increased in nonalcoholic fatty liver disease (NAFLD), but its relationship with liver inflammation is not defined.

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          The portal inflammatory infiltrate and ductular reaction in human nonalcoholic fatty liver disease.

          Victoria L. Gadd, Richard Skoien, Elizabeth E. Powell … (2014)
          Although nonalcoholic fatty liver disease (NAFLD) is conventionally assessed histologically for lobular features of inflammation, development of portal fibrosis appears to be associated with disease progression. We investigated the composition of the portal inflammatory infiltrate and its relationship to the ductular reaction (DR), a second portal phenomenon implicated in fibrogenesis. The portal inflammatory infiltrate may contribute directly to fibrogenesis as well as influence the fate of the DR hepatic progenitor cells (HPCs), regulating the balance between liver repair and fibrosis. The presence of portal inflammation in NAFLD was strongly correlated with disease severity (fibrosis stage) and the DR. The portal infiltrate was characterized by immunostaining NAFLD liver biopsy sections (n = 33) for broad leukocyte subset markers (CD68, CD3, CD8, CD4, CD20, and neutrophil elastase) and selected inflammatory markers (matrix metalloproteinase 9 and interleukin [IL]-17). Cells expressing all markers examined were identified throughout the liver lobules and in portal tracts, although portal tracts were more densely populated (P < 0.01), and dominated by CD68(+) macrophages and CD8(+) lymphocytes, at all stages of disease. An increase in portal macrophages in NAFLD patients with steatosis alone (P < 0.01) was the earliest change detected, even before elevated expression of the proinflammatory cytokines, IL1B and TNF, in patients with early NASH (P < 0.05). Portal and periductal accumulation of all other cell types examined occurred in progressed NASH (all P < 0.05). Knowledge of the complex cellular composition of the portal inflammatory infiltrate and HPC/DR niche in NAFLD will shape future functional studies to elucidate the contribution of portal inflammation to HPC differentiation and NAFLD pathogenesis. © 2014 by the American Association for the Study of Liver Diseases.
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            A human hepatocellular in vitro model to investigate steatosis.

            Maria José Gómez-Lechón, María Teresa Donato, Alicia Martínez-Romero … (2007)
            The present study was designed to define an experimental model of hepatocellular steatosis with a fat overaccumulation profile in which the metabolic and cytotoxic/apoptotic effects could be separated. This was accomplished by defining the experimental conditions of lipid exposure that lead to significant intracellular fat accumulation in the absence of overt cytotoxicity, therefore allowing to differentiate between cytotoxic and apoptotic effects. Palmitic (C16:0) and oleic (C18:1) acids are the most abundant fatty acids (FFAs) in liver triglycerides in both normal subjects and patients with nonalcoholic fatty liver disease (NAFLD). Therefore, human hepatocytes and HepG2 cells were incubated with a mixture of different proportions of saturated (palmitate) and unsaturated (oleate) FFAs to induce fat-overloading. Similar intracellular levels of lipid accumulation as in the human steatotic liver were achieved. Individual FFAs have a distinct inherent toxic potential. Fat accumulation, cytotoxicity and apoptosis in cells exposed to the FFA mixtures were investigated. The FFA mixture containing a low proportion of palmitic acid (oleate/palmitate, 2:1 ratio) is associated with minor toxic and apoptotic effects, thus representing a cellular model of steatosis that mimics benign chronic steatosis. On the other hand, a high proportion of palmitic acid (oleate/palmitate, 0:3 ratio) might represent a cellular model of steatosis in which saturated FFAs promote an acute harmful effect of fat overaccumulation in the liver. These hepatic cellular models are apparently suitable to experimentally investigate the impact of fat overaccumulation in the liver excluding other factors that could influence hepatocyte behaviour.
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              Gut--liver axis: the impact of gut microbiota on non alcoholic fatty liver disease.

              D Compare, P Coccoli, A. Rocco … (2012)
              To examine the impact of gut microbiota on non alcoholic fatty liver disease (NAFLD) pathogenesis. Emerging evidence suggests a strong interaction between gut microbiota and liver. Receiving approximately 70% of its blood supply from the intestine, the liver represents the first line of defence against gut-derived antigens. Intestinal bacteria play a key role in the maintenance of gut-liver axis health. Disturbances in the homeostasis between bacteria- and host-derived signals at the epithelial level lead to a break in intestinal barrier function and may foster "bacterial translocation", defined as the migration of bacteria or bacterial products from the intestinal lumen to mesenteric lymph nodes or other extraintestinal organs and sites. While the full repertoire of gut-derived microbial products that reach the liver in health and disease has yet to be explored, the levels of bacterial lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, are increased in the portal and/or systemic circulation in several types of chronic liver diseases. Derangement of the gut flora, particularly small intestinal bacterial overgrowth, occurs in a large percentage (20-75%) of patients with chronic liver disease. In addition, evidence implicating the gut-liver axis in the pathogenesis of metabolic liver disorders has accumulated over the past ten years. Complex metabolic diseases are the product of multiple perturbations under the influence of triggering factors such as gut microbiota and diet, thus, modulation of the gut microbiota may represent a new way to treat or prevent NAFLD. Copyright © 2012 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Guido Carpino: (View ORCID Profile)
                Daniele Pastori: (View ORCID Profile)
                Diletta Overi: (View ORCID Profile)
                Journal
                Title: Hepatology
                Abbreviated Title: Hepatology
                Publisher: Wiley
                ISSN (Print): 0270-9139
                ISSN (Electronic): 1527-3350
                Publication date Created: August 2020
                Publication date (Electronic): May 22 2020
                Publication date (Print): August 2020
                Volume: 72
                Issue: 2
                Pages: 470-485
                Affiliations
                [1 ]Department of Movement Human and Health Sciences Division of Health Sciences University of Rome “Foro Italico,” Rome Italy
                [2 ]Department of Internal Medicine and Medical Specialties Sapienza University of Rome Rome Italy
                [3 ]Department of Medico‐Surgical Sciences and Biotechnologies Sapienza University of Rome Latina Italy
                [4 ]Mediterranea Cardiocentro Naples Italy
                [5 ]Department of Anatomical Histological Forensic Medicine and Orthopedics Sciences Sapienza University of Rome Rome Italy
                [6 ]Indiana Center for Liver Research Richard L. Roudebush VA Medical Center and Indiana University Indianapolis IN
                [7 ]Department of Precision and Translational Medicine Sapienza University of Rome Rome Italy
                [8 ]Department of General Surgery and Surgical Specialty Paride Stefanini Sapienza University of Rome Rome Italy
                [9 ]Department of Gastroenterology and Hepatology Marche Polytechnic University Ancona Italy
                [10 ]Department of Public Health and Infectious Diseases Sapienza University of Rome Rome Italy
                Article
                DOI: 10.1002/hep.31056
                PubMed ID: 31808577
                SO-VID: b895810f-235c-4310-9ced-7188efadfd2a
                Copyright © © 2020
                License:

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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