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Cells
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The Inflammation in Acute and Chronic Liver Injury
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The Inflammation in Acute and Chronic Liver Injury

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 2797

Special Issue Editors

Dr. Fabrizio Bronte

E-Mail Website
Guest Editor
Ospedali Riuniti Villa Sofia-V. Cervello, Università degli Studi di Palermo, Palermo, Italy
Interests: liver and biliary cancer; hepatitis; autoimmune
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppe Mogavero

E-Mail
Guest Editor
Ospedali Riuniti Villa Sofia-V. Cervello, Università degli Studi di Palermo, Palermo, Italy
Interests: liver and biliary cancer; hepatitis; autoimmune; endoscopy

Special Issue Information

Dear Colleagues,

Acute and chronic liver diseases are supported by various etiological agents: viral, such as hepatitis B virus (HBV) and hepatitis C virus (HCV) infections; metabolic, such as non-alcoholic steatohepatitis (NASH) and alcoholic hepatitis (ASH); autoimmune diseases, such as autoimmune hepatitis (AE), primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC); accumulation forms, such as hemochromatosis (HE) and Wilson's disease (WD). These forms of liver diseases recognize a well-determined pathophysiological mechanism, in which the etiological insult determines an inflammatory cascade, acute or chronic, which can lead, in the long term, to fibrosis and, therefore, to cirrhosis with its complications. Hepatocyte damage induced by etiological agents stimulates inflammation and triggers the activation of immune cells resident in the liver. Among these, Kupffer cells, liver-resident macrophages, but also other inflammatory cells, such as infiltrating macrophages, T lymphocytes, neutrophils and dendritic cells (DCs), play an important role. This process activates hepatic stellate cells, which are the main source of myofibroblasts in the liver. In this Special Issue, we want to explore the mechanisms underlying the hepatic inflammatory processes involved in acute and continuous forms.

Dr. Fabrizio Bronte
Dr. Giuseppe Mogavero
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • liver
  • HBV
  • HCV
  • NASH
  • autoimmune
  • fibrosis
  • inflammation
  • hepatitis
  • acute hepatitis
  • chronic hepatitis
  • cirrhosis

Published Papers (2 papers)

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Research

11 pages, 3266 KiB  
Article
Effect of Low Testosterone Levels on the Expression of Proliferator-Activated Receptor Alpha in Female Patients with Primary Biliary Cholangitis
by Agnieszka Kempińska-Podhorodecka, Joanna Abramczyk, Eliza Cielica, Bartosz Huła, Hanna Maciejowska, Jesus Banales, Piotr Milkiewicz and Małgorzata Milkiewicz
Cells 2023, 12(18), 2273; https://doi.org/10.3390/cells12182273 - 14 Sep 2023
Cited by 2 | Viewed by 1026
Abstract
Sex-dependent patterns in chronic immune-mediated cholangiopathies, like primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC), remain poorly understood. Peroxisome proliferator-activated receptor alpha (PPAR-α), expressed in immune cells, plays a key role in innate defence. In this study, the relationship between PPAR-α expression [...] Read more.
Sex-dependent patterns in chronic immune-mediated cholangiopathies, like primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC), remain poorly understood. Peroxisome proliferator-activated receptor alpha (PPAR-α), expressed in immune cells, plays a key role in innate defence. In this study, the relationship between PPAR-α expression in peripheral blood mononuclear cells (PBMCs), serum androgen levels, IFNγ production, and sex-dependent tendencies during the development of PBC and PSC was investigated. We confirmed that normal cholangiocytes respond to PPAR-α and inhibit the lipopolysaccharide-induced expression of IL-6, IL-1b, and TNFα. Compared with PSC patients, PPAR-α was downregulated, while IFNγ was upregulated, in the PBMCs of PBC patients. When the analysis was conducted on females only, there was no difference in PPAR-α, but IFNγ was elevated in females with PBC compared with those with PSC. Serum testosterone concentrations in females with PBC were below the normal range (regardless of age) and correlated positively with PPAR-α and negatively with IFNγ. While PPAR-α has been reported to be a target of miR-155 and miR-21, no correlations with these microRNAs were observed in the PBMCs. However, a positive correlation between miR-21 and IFNγ was observed. Our results showed suppressed PPAR-α expression accompanied by reduced testosterone levels in women with PBC, which should elicit interest in the role of testosterone in PBC development. Full article
(This article belongs to the Special Issue The Inflammation in Acute and Chronic Liver Injury)
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17 pages, 2453 KiB  
Article
Endotoxemia Associated with Liver Disease Correlates with Systemic Inflammation and T Cell Exhaustion in Hepatitis C Virus Infection
by Carey L. Shive, Corinne M. Kowal, Alexandra F. Desotelle, Ynez Nguyen, Sarah Carbone, Lenche Kostadinova, Perica Davitkov, Megan O’Mara, Alexandra Reihs, Hinnah Siddiqui, Brigid M. Wilson and Donald D. Anthony
Cells 2023, 12(16), 2034; https://doi.org/10.3390/cells12162034 - 10 Aug 2023
Cited by 1 | Viewed by 1409
Abstract
Both acute and chronic hepatitis C virus (HCV) infections are characterized by inflammation. HCV and reduced liver blood filtration contribute to inflammation; however, the mechanisms of systemic immune activation and dysfunction as a result of HCV infection are not clear. We measured circulating [...] Read more.
Both acute and chronic hepatitis C virus (HCV) infections are characterized by inflammation. HCV and reduced liver blood filtration contribute to inflammation; however, the mechanisms of systemic immune activation and dysfunction as a result of HCV infection are not clear. We measured circulating inflammatory mediators (IL-6, IP10, sCD163, sCD14), indices of endotoxemia (EndoCab, LBP, FABP), and T cell markers of exhaustion and senescence (PD-1, TIGIT, CD57, KLRG-1) in HCV-infected participants, and followed a small cohort after direct-acting anti-viral therapy. IL-6, IP10, Endocab, LBP, and FABP were elevated in HCV participants, as were T cell co-expression of exhaustion and senescence markers. We found positive associations between IL-6, IP10, EndoCab, LBP, and co-expression of T cell markers of exhaustion and senescence. We also found numerous associations between reduced liver function, as measured by plasma albumin levels, and T cell exhaustion/senescence, inflammation, and endotoxemia. We found positive associations between liver stiffness (TE score) and plasma levels of IL-6, IP10, and LBP. Lastly, plasma IP10 and the proportion of CD8 T cells co-expressing PD-1 and CD57 decreased after initiation of direct-acting anti-viral therapy. Although associations do not prove causality, our results support the model that translocation of microbial products, resulting from decreased liver blood filtration, during HCV infection drives chronic inflammation that results in T cell exhaustion/senescence and contributes to systemic immune dysfunction. Full article
(This article belongs to the Special Issue The Inflammation in Acute and Chronic Liver Injury)
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