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      • Record: found
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      Is Open Access

      Complements are involved in alcoholic fatty liver disease, hepatitis and fibrosis

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          Abstract

          The complement system is a key component of the body’s immune system. When abnormally activated, this system can induce inflammation and damage to normal tissues and participate in the development and progression of a variety of diseases. In the past, many scholars believed that alcoholic liver disease (ALD) is induced by the stress of ethanol on liver cells, including oxidative stress and dysfunction of mitochondria and protease bodies, causing hepatocyte injury and apoptosis. Recent studies have shown that complement activation is also involved in the genesis and development of ALD. This review focuses on the roles of complement activation in ALD and of therapeutic intervention in complement-activation pathways. We intend to provide new ideas on the diagnosis and treatment of ALD.

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          Most cited references80

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          The inflammasomes: guardians of the body.

          Fabio Martinon, Annick Mayor, Jurg Tschopp (2009)
          The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and to eliminate them. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes called inflammasomes that link the sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammatory cytokines IL-1beta and IL-18. The NALP3 inflammasome has been associated with several autoinflammatory conditions including gout. Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response. In this review, we discuss the role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease.
          Article 0 comments Cited 688 times – based on 0 reviews     Review now
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            Role of C5a in inflammatory responses.

            Ren-Feng Guo, Peter Ward (2005)
            The complement system not only represents an effective innate immune mechanism of host defense to eradicate microbial pathogens, but it is also widely involved in many forms of acute and chronic inflammatory diseases including sepsis, acute lung injury, ischemia-reperfusion injury, and asthma, to give just a few examples. The complement-activated product, C5a, displays powerful biological activities that lead to inflammatory sequelae. C5a is a strong chemoattractant and is involved in the recruitment of inflammatory cells such as neutrophils, eosinophils, monocytes, and T lymphocytes, in activation of phagocytic cells and release of granule-based enzymes and generation of oxidants, all of which may contribute to innate immune functions or tissue damage. Accumulating data suggest that C5a provides a vital bridge between innate and adaptive immune functions, extending the roles of C5a in inflammation. Herein, we review human and animal data describing the cellular and molecular mechanisms of C5a in the development of inflammatory disorders, sepsis, acute lung injury, ischemia-reperfusion injury, and asthma.
            Article 0 comments Cited 275 times – based on 0 reviews     Review now
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              Selective depletion of macrophages reveals distinct, opposing roles during liver injury and repair.

              Jeremy Duffield, Stuart J Forbes, Christothea M. Constandinou … (2005)
              Macrophages perform both injury-inducing and repair-promoting tasks in different models of inflammation, leading to a model of macrophage function in which distinct patterns of activation have been proposed. We investigated macrophage function mechanistically in a reversible model of liver injury in which the injury and recovery phases are distinct. Carbon tetrachloride---induced liver fibrosis revealed scar-associated macrophages that persisted throughout recovery. A transgenic mouse (CD11b-DTR) was generated in which macrophages could be selectively depleted. Macrophage depletion when liver fibrosis was advanced resulted in reduced scarring and fewer myofibroblasts. Macrophage depletion during recovery, by contrast, led to a failure of matrix degradation. These data provide the first clear evidence that functionally distinct subpopulations of macrophages exist in the same tissue and that these macrophages play critical roles in both the injury and recovery phases of inflammatory scarring.
              Article 0 comments Cited 243 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Cheng-Jie Lin
                Zhi-Gao Hu
                Guan-Dou Yuan
                Biao Lei
                Song-Qing He
                Journal
                Journal ID (nlm-ta): World J Hepatol
                Journal ID (publisher-id): WJH
                Title: World Journal of Hepatology
                Publisher: Baishideng Publishing Group Inc
                ISSN (Electronic): 1948-5182
                Publication date (Print): 27 October 2018
                Publication date (Electronic): 27 October 2018
                Volume: 10
                Issue: 10
                Pages: 662-669
                Affiliations
                Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
                Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
                Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
                Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
                Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China. dr_hesongqing@ 123456163.com
                Author notes

                Author contributions: Lin CJ and Hu ZG contributed equally to this work; He SQ designed research; Lin CJ, Hu ZG and Yuan GD searched the relevant literatures; and Lin CJ wrote the review; Lei B and He SQ revised the review.

                Supported by State Key Program of National Natural Science Foundation of China, No. 8143000311; National Natural Science Foundation of China, No. 81660103 and No. 81771674; 111 Project, No. D17011; Guangxi BaGui Scholars; the Natural Science Foundation of Guangxi Province, No. 2015GXNSFFA139004.

                Correspondence to: Song-Qing He, PhD, Chief Doctor, Professor, Research Professor, Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. dr_hesongqing@ 123456163.com

                Telephone: +86-771-5356568

                Article
                Other ID: jWJH.v10.i10.pg662
                DOI: 10.4254/wjh.v10.i10.662
                PMC ID: 6206158
                PubMed ID: 30386459
                SO-VID: d630abde-48df-41b2-958d-a426394c6f49
                Copyright © ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                Date received : 10 April 2018
                Date revision received : 26 July 2018
                Date accepted : 1 August 2018
                Categories
                Subject: Review

                Keywords: alcoholic liver disease,complement system proteins,complement regulator,liver cells,hepatocyte injury
                Data availability:
                Keywords: alcoholic liver disease, complement system proteins, complement regulator, liver cells, hepatocyte injury

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