Development of Kupffer cell targeting type-I interferon for the treatment of hepatitis via inducing anti-inflammatory and immunomodulatory actions

Minayoshi, Yuki; Maeda, Hitoshi; Yanagisawa, Hiroki; Hamasaki, Koji; Mizuta, Yuki; Nishida, Kimiaki; Kinoshita, Ryô; Enoki, Yuki; Imafuku, Tadasi; Chuang, Victor Tuan Giam; Koga, Tomoaki; Fujiwara, Yukio; Takeya, Motohiro; Sonoda, Kayoko; Wakayama, Tomohiko; Taguchi, Kazuaki; Ishima, Yu; Ishida, Tatsuhiro; Iwakiri, Yasuko; Tanaka, Motohiko; Sasaki, Yutaka; Watanabe, Hiroshi; Otagiri, Masaki; Maruyama, Toru

doi:10.1080/10717544.2018.1464083

Cited by 11 publications

(7 citation statements)

References 35 publications

(44 reference statements)

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“…Both academia and industry have used various approaches to develop novel albumin-associated pharmaceutical preparations: (i) albumin-drug conjugation to prolong blood retention [ 11 , 12 , 13 , 14 , 15 ], (ii) nanoparticulation by albumin aggregates to improve stability and the loading efficiency of hydrophobic substances [ 16 , 17 , 18 ], (iii) liposome, micelles, niosomes, and emulsions fused with albumin to compensate for their drawbacks [ 19 , 20 , 21 , 22 , 23 ]. Among these approaches, adapting albumin for use in a liposome-based drug delivery system (DDS) has shown promising results.…”

Section: Introductionmentioning

confidence: 99%

“…These preparations take advantage of the following inherent structural and physiological characteristics of albumin-Albumin has a good biocompatibility with a long plasma half-life, the aqueous solubility of endogenous and exogenous hydrophobic substances can be improved by their binding to albumin, and the cysteine residue at position 34 of albumin readily reacts with oxidative products and other thiol groups (Figure 1). Both academia and industry have used various approaches to develop novel albuminassociated pharmaceutical preparations: (i) albumin-drug conjugation to prolong blood retention [11][12][13][14][15], (ii) nanoparticulation by albumin aggregates to improve stability and the loading efficiency of hydrophobic substances [16][17][18], (iii) liposome, micelles, niosomes, and emulsions fused with albumin to compensate for their drawbacks [19][20][21][22][23]. Among these approaches, adapting albumin for use in a liposome-based drug delivery system (DDS) has shown promising results.…”

Section: Introductionmentioning

confidence: 99%

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When Albumin Meets Liposomes: A Feasible Drug Carrier for Biomedical Applications

et al. 2021

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Albumin, the most abundant protein in plasma, possesses some inherent beneficial structural and physiological characteristics that make it suitable for use as a drug delivery agent, such as an extraordinary drug-binding capacity and long blood retention, with a high biocompatibility. The use of these characteristics as a nanoparticle drug delivery system (DDS) offers several advantages, including a longer circulation time, lower toxicity, and more significant drug loading. To date, many innovative liposome preparations have been developed in which albumin is involved as a DDS. These novel albumin-containing liposome preparations show superior deliverability for genes, hydrophilic/hydrophobic substances and proteins/peptides to the targeting area compared to original liposomes by virtue of their high biocompatibility, stability, effective loading content, and the capacity for targeting. This review summarizes the current status of albumin applications in liposome-based DDS, focusing on albumin-coated liposomes and albumin-encapsulated liposomes as a DDS carrier for potential medical applications.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

When Albumin Meets Liposomes: A Feasible Drug Carrier for Biomedical Applications

et al. 2021

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“…In addition to macrophages, NKT, NK, T cells, and myeloid‐derived suppressor cells play important roles in acute liver injury 39–41 . Hence, the proportions of NKT (CD3 + NK1.1 + ), NK (CD3 − NK1.1 + ), T (CD3 + NK1.1 − ), and myeloid‐derived suppressor cells (MDSCs, CD11b + Gr‐1 + ) cells in the liver were measured using flow cytometry (detailed flow gate strategies are shown in Figure S8).…”

Section: Resultsmentioning

confidence: 99%

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

Zhang,

Cheng,

Zhang

et al. 2024

The FASEB Journal

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Immune‐mediated acute hepatic injury is characterized by the destruction of a large number of hepatocytes and severe liver function damage. Interleukin‐28A (IL‐28A), a member of the IL‐10 family, is notable for its antiviral properties. However, despite advances in our understanding of IL‐28A, its role in immune‐mediated acute injury remains unclear. The present study investigated the role of IL‐28A in concanavalin A (Con A)‐induced acute immune liver injury. After Con A injection in mice, IL‐28A level significantly increased. IL‐28A deficiency was found to protect mice from acute liver injury, prolong survival time, and reduce serum aspartate aminotransferase and alanine aminotransferase levels. In contrast, recombinant IL‐28A aggravated liver injury in mice. The proportion of activated M1 macrophages was significantly lower in the IL‐28A‐deficiency group than in the wild‐type mouse group. In adoptive transfer experiments, M1 macrophages from WT could exacerbate mice acute liver injury symptoms in the IL‐28A deficiency group. Furthermore, the expression of proinflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), IL‐12, IL‐6, and IL‐1β, by M1 macrophages decreased significantly in the IL‐28A‐deficiency group. Western blotting demonstrated that IL‐28A deficiency could limit M1 macrophage polarization by modulating the nuclear factor (NF)‐κB, mitogen‐activated protein kinase (MAPK), and interferon regulatory factor (IRF) signaling pathways. In summary, IL‐28A deletion plays an important protective role in the Con A‐induced acute liver injury model and IL‐28A deficiency inhibits the activation of M1 macrophages by inhibiting the NF‐κB, MAPK, and IRF signaling pathways. These results provide a potential new target for the treatment of immune‐related hepatic injury.

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“…Soluble inflammatory mediators including interleukins have been implicated in ALD[ 60 , 89 , 90 ] and are associated with outcome in patients with AH[ 91 ]. Elevated serum IL-6 levels have recently been identified as a predictor of mortality in severe AH patients[ 64 ].…”

Section: Cell Signaling Pathwaysmentioning

confidence: 99%

Oxidative stress in alcohol-related liver disease

Tan

Yates

Lilly

et al. 2020

WJH

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Alcohol consumption is one of the leading causes of the global burden of disease and results in high healthcare and economic costs. Heavy alcohol misuse leads to alcohol-related liver disease, which is responsible for a significant proportion of alcohol-attributable deaths globally. Other than reducing alcohol consumption, there are currently no effective treatments for alcohol-related liver disease. Oxidative stress refers to an imbalance in the production and elimination of reactive oxygen species and antioxidants. It plays important roles in several aspects of alcohol-related liver disease pathogenesis. Here, we review how chronic alcohol use results in oxidative stress through increased metabolism via the cytochrome P450 2E1 system producing reactive oxygen species, acetaldehyde and protein and DNA adducts. These trigger inflammatory signaling pathways within the liver leading to expression of pro-inflammatory mediators causing hepatocyte apoptosis and necrosis. Reactive oxygen species exposure also results in mitochondrial stress within hepatocytes causing structural and functional dysregulation of mitochondria and upregulating apoptotic signaling. There is also evidence that oxidative stress as well as the direct effect of alcohol influences epigenetic regulation. Increased global histone methylation and acetylation and specific histone acetylation inhibits antioxidant responses and promotes expression of key pro-inflammatory genes. This review highlights aspects of the role of oxidative stress in disease pathogenesis that warrant further study including mitochondrial stress and epigenetic regulation. Improved understanding of these processes may identify novel targets for therapy.

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Development of Kupffer cell targeting type-I interferon for the treatment of hepatitis via inducing anti-inflammatory and immunomodulatory actions

Cited by 11 publications

References 35 publications

When Albumin Meets Liposomes: A Feasible Drug Carrier for Biomedical Applications

When Albumin Meets Liposomes: A Feasible Drug Carrier for Biomedical Applications

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

Oxidative stress in alcohol-related liver disease

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