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The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases
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The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 10 May 2024 | Viewed by 5578

Special Issue Editors

Dr. Young-Su Yi

E-Mail Website
Guest Editor
Department of Life Sciences, Kyonggi University, Suwon 16227, Republic of Korea
Interests: inflammation; inflammatory/autoimmune diseases; non-canonical inflammasomes; macrophage; anti-inflammatory therapeutics, signaling transduction; immunology; molecular biology; biochemistry
Special Issues, Collections and Topics in MDPI journals
Dr. Miyong Yun

E-Mail Website
Guest Editor
Faculty of Molecular Biology, Sejong University, Seoul 05006, Republic of Korea
Interests: zerumbone; ETBF; BFT; inflammation; nf-κb
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is an innate immune response to protect our body from various pathogens and cellular dangers; however, chronic inflammation, which is a repeated and prolonged inflammation, is considered a critical risk factor for numerous diseases, including liver diseases. An inflammatory response consists of two successive steps, the ‘priming’ and ‘triggering’ steps, which are preparation and activation processes of inflammatory responses, respectively. The cardinal feature of the priming step is transcriptional activation of inflammatory molecules, while the key process of the triggering step is the activation of inflammasomes, intracellular protein complexes that provide a platform of the inflammatory responses. Previous studies have demonstrated that inflammation and inflammasome activation play roles in liver diseases, which provides strong evidence that inflammasomes are central players in inflammatory responses and liver diseases and may be new potential targets for developing novel therapeutics against liver diseases. However, the roles of inflammasomes and their dysregulation during inflammatory responses and liver diseases still remain to be investigated.

This Special Issue welcomes studies exploring, but not limited to, the regulatory roles of inflammasomes in inflammatory responses and liver diseases, such as non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hepatitis, fibrosis, cirrhosis, liver injuries, and hepatocellular carcinomas (HCCs), identifying and validating novel targets regulating inflammasome functions, and potential inflammasome-targeted therapeutics.

Dr. Young-Su Yi
Dr. Miyong Yun
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • inflammation
  • inflammasome
  • inflammatory responses
  • liver diseases

Published Papers (4 papers)

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Research

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16 pages, 3313 KiB  
Article
Overexpression of Interleukin-8 Promotes the Progression of Fatty Liver to Nonalcoholic Steatohepatitis in Mice
by Ye Eun Cho, Yeonsoo Kim, Seung-Jin Kim, Haeseung Lee and Seonghwan Hwang
Int. J. Mol. Sci. 2023, 24(20), 15489; https://doi.org/10.3390/ijms242015489 - 23 Oct 2023
Cited by 4 | Viewed by 1283
Abstract
Nonalcoholic steatohepatitis (NASH) is an advanced stage of fatty liver disease characterized by liver damage, inflammation, and fibrosis. Although neutrophil infiltration is consistently observed in the livers of patients with NASH, the precise role of neutrophil-recruiting chemokines and infiltrating neutrophils in NASH pathogenesis [...] Read more.
Nonalcoholic steatohepatitis (NASH) is an advanced stage of fatty liver disease characterized by liver damage, inflammation, and fibrosis. Although neutrophil infiltration is consistently observed in the livers of patients with NASH, the precise role of neutrophil-recruiting chemokines and infiltrating neutrophils in NASH pathogenesis remains poorly understood. Here, we aimed to elucidate the role of neutrophil infiltration in the transition from fatty liver to NASH by examining hepatic overexpression of interleukin-8 (IL8), a major chemokine responsible for neutrophil recruitment in humans. Mice fed a high-fat diet (HFD) for 3 months developed fatty liver without concurrent liver damage, inflammation, and fibrosis. Subsequent infection with an adenovirus overexpressing human IL8 for an additional 2 weeks increased IL8 levels, neutrophil infiltration, and liver injury in mice. Mechanistically, IL8-induced liver injury was associated with the upregulation of components of the NADPH oxidase 2 complex, which participate in neutrophil oxidative burst. IL8-driven neutrophil infiltration promoted macrophage aggregate formation and upregulated the expression of chemokines and inflammatory cytokines. Notably, IL8 overexpression amplified factors associated with fibrosis, including collagen deposition and hepatic stellate cell activation, in HFD-fed mice. Collectively, hepatic overexpression of human IL8 promotes neutrophil infiltration and fatty liver progression to NASH in HFD-fed mice. Full article
(This article belongs to the Special Issue The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases)
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14 pages, 3471 KiB  
Article
Activation of NLRP3 Inflammasome in Liver of Long Evans Lactating Rats and Its Perinatal Effects in the Offspring after Bisphenol F Exposure
by Beatriz Linillos-Pradillo, Sergio D. Paredes, María Ortiz-Cabello, Margret Schlumpf, Walter Lichtensteiger, Elena Vara, Jesús A. F. Tresguerres and Lisa Rancan
Int. J. Mol. Sci. 2023, 24(18), 14129; https://doi.org/10.3390/ijms241814129 - 15 Sep 2023
Cited by 2 | Viewed by 777
Abstract
The liver is the organ responsible for the metabolism and detoxification of BPF, the BPA analogue that is replacing it in plastic-based products. It is not known whether BPF can trigger inflammatory responses via the NLRP3 inflammasome, which plays a major role in [...] Read more.
The liver is the organ responsible for the metabolism and detoxification of BPF, the BPA analogue that is replacing it in plastic-based products. It is not known whether BPF can trigger inflammatory responses via the NLRP3 inflammasome, which plays a major role in the development of liver disease. The aim of this study was to evaluate nitrosative stress species (RNS) and NLRP3 inflammasome activation in the liver of lactating dams after BPF exposure. Moreover, it was studied whether this effect could also be observed in the liver of female and male offspring at postnatal day 6 (PND6). 36 Long Evans rats were randomly distributed according to oral treatment into three groups: Control, BPF-low dose (LBPF; 0.0365 mg/kg b.w./day) group and BPF-high dose (HBPF; 3.65 mg/kg b.w./day) group. The levels of nitrosative stress-inducing proteins (eNOS, iNOS, HO-1d), NLRP3 inflammasome components (NLRP3, PyCARD, CASP1) and proinflammatory cytokines (IL-1β, IL-18, IFN-γ and TNF-α) were measured by gene and protein expression in the liver of lactating dams and in female and male PND6 offspring. Lactating dams treated with LBPF showed a significant increase in iNOS and HO-1d, activation of NLRP3 components (NLRP3, PyCARD, CASP1) and promoted the release of proinflammatory cytokines such as IL-1β, IL-18, IFN-γ and TNF-α. Similar effects were found in female and male PND6 offspring after perinatal exposure. LBPF oral administration and perinatal exposure caused an increase of nitrosative stress markers and proinflammatory cytokines. Also, NLRP3 inflammasome activation was significantly increased in in the liver of lactating dams and PND6 offspring. Full article
(This article belongs to the Special Issue The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases)
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14 pages, 7605 KiB  
Article
CXCL5 Promotes Acetaminophen-Induced Hepatotoxicity by Activating Kupffer Cells
by Kexin Qiu, Yan Pan, Weizhi Huang, Mengyuan Li, Xueqing Yan, Zixiong Zhou and Jing Qi
Int. J. Mol. Sci. 2023, 24(15), 12180; https://doi.org/10.3390/ijms241512180 - 29 Jul 2023
Viewed by 1472
Abstract
Kupffer cells (KCs) play a key part in the pathological process of acetaminophen (APAP)-induced acute liver injury (ALI), the leading cause of acute liver failure in the world. CXC motif chemokine ligand 5 (CXCL5) exerts proinflammatory effects in acute respiratory distress syndrome and [...] Read more.
Kupffer cells (KCs) play a key part in the pathological process of acetaminophen (APAP)-induced acute liver injury (ALI), the leading cause of acute liver failure in the world. CXC motif chemokine ligand 5 (CXCL5) exerts proinflammatory effects in acute respiratory distress syndrome and arthritis. In the current study, we aim to reveal the effects of CXCL5 on the activation of KCs and the role of CXCL5 in the pathogenesis of APAP-induced hepatotoxicity. The in vivo study, conducted on mice intraperitoneally injected with APAP (300 mg/kg) to establish the ALI model and then treated with Anti-CXCL5 mAb at 30 min and 12 h after the APAP challenge, showed that CXCL5 expression significantly increased in injured livers, and Anti-CXCL5 mAb mitigated the degree of APAP-evoked ALI in mice which was proven through biochemicals and histological examination. Also, neutralization of CXCL5 had no significant effect on APAP metabolism in the liver but exhibited anti-inflammatory effects and ameliorated hepatocellular death in the injured liver. The in vitro data displayed that recombinant mouse CXCL5 treatment promoted APAP-induced cellular toxicity in primary hepatocytes co-cultured with KCs, compared with single-cultured hepatocytes. Consistent with the result, we found that the Anti-CXCL5 mAb gradient decreased LPS-induced expression of inflammatory cytokines in single-cultured KCs. Therefore, CXCL5 could stimulate KCs to produce inflammatory mediators, therefore damaging hepatocytes from APAP toxicity. Full article
(This article belongs to the Special Issue The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases)
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Review

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21 pages, 2044 KiB  
Review
Regulatory Roles of Flavonoids in Caspase-11 Non-Canonical Inflammasome-Mediated Inflammatory Responses and Diseases
by Young-Su Yi
Int. J. Mol. Sci. 2023, 24(12), 10402; https://doi.org/10.3390/ijms241210402 - 20 Jun 2023
Cited by 5 | Viewed by 1357
Abstract
Inflammasomes are multiprotein complexes that activate inflammatory responses by inducing pyroptosis and secretion of pro-inflammatory cytokines. Along with many previous studies on inflammatory responses and diseases induced by canonical inflammasomes, an increasing number of studies have demonstrated that non-canonical inflammasomes, such as mouse [...] Read more.
Inflammasomes are multiprotein complexes that activate inflammatory responses by inducing pyroptosis and secretion of pro-inflammatory cytokines. Along with many previous studies on inflammatory responses and diseases induced by canonical inflammasomes, an increasing number of studies have demonstrated that non-canonical inflammasomes, such as mouse caspase-11 and human caspase-4 inflammasomes, are emerging key players in inflammatory responses and various diseases. Flavonoids are natural bioactive compounds found in plants, fruits, vegetables, and teas and have pharmacological properties in a wide range of human diseases. Many studies have successfully demonstrated that flavonoids play an anti-inflammatory role and ameliorate many inflammatory diseases by inhibiting canonical inflammasomes. Others have demonstrated the anti-inflammatory roles of flavonoids in inflammatory responses and various diseases, with a new mechanism by which flavonoids inhibit non-canonical inflammasomes. This review discusses recent studies that have investigated the anti-inflammatory roles and pharmacological properties of flavonoids in inflammatory responses and diseases induced by non-canonical inflammasomes and further provides insight into developing flavonoid-based therapeutics as potential nutraceuticals against human inflammatory diseases. Full article
(This article belongs to the Special Issue The Regulatory Roles of Inflammation and Inflammasomes in Liver Diseases)
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