Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

Taniki, Nobuhito; Nakamoto, Nobuhiro; Chu, Po–Sung; Mikami, Yohei; Amiya, Takeru; Teratani, Toshiaki; Suzuki, Takahiro; Tsukimi, Tomoya; Fukuda, Shinji; Yamaguchi, Akihiro; Shiba, Shintaro; Miyake, Rei; Katayama, Tadashi; Ebinuma, Hirotoshi; Kanai, Takanori

doi:10.1172/jci.insight.91980

Cited by 25 publications

(15 citation statements)

References 43 publications

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“…fraction was prepared from intestinal tissues by digestion with HBSS (Nacalai Tesque) containing 1 mM dithiothreitol (Sigma-Aldrich) and 5 mM EDTA (Gibco, Thermo Fisher Scientific) for 30 minutes at 37°C. Subsequently, the lamina propria fraction was prepared by digestion with a digestion solution containing 1.5% FBS, 1.0 mg/mL collagenase A (Roche Diagnostics GmbH), and 0.1 mg/mL DNase (Sigma-Aldrich) for 30 minutes at 37°C as described previously (45). Cells from each tissue were suspended in 40% Percoll and overlaid on a 75% Percoll fraction.…”

Section: Discussionmentioning

confidence: 99%

Plasmacytoid dendritic cells protect against immune-mediated acute liver injury via IL-35

Koda¹,

Nakamoto²,

Chu³

et al. 2019

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

Plasmacytoid dendritic cells protect against immune-mediated acute liver injury via IL-35

Koda¹,

Nakamoto²,

Chu³

et al. 2019

Journal of Clinical Investigation

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“…These conflict phenotypes may be resulted from the difference of microbiota abundance between GF and antibiotics treated mice. Nobuhito et al showed that inducing colitis with DSS for 7 days led to intestinal leakage, exposed intestinal microbes to the systemic immune cells and the liver through the portal vein, induced a systemic immune tolerance, and thereby reduced Con A-induced liver damage (Taniki et al, 2018 ).…”

Section: The Gut Microbiota and Con A-induced Autoimmune Hepatitismentioning

confidence: 99%

Gut Microbiota and Chemical-Induced Acute Liver Injury

Chen

2021

Front. Physiol.

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Background: Drug overdose or chemical exposures are the main causes of acute liver injury (ALI). Severe liver injury can develop into liver failure that is an important cause of liver-related mortality in intensive care units in most countries. Pharmacological studies have utilized a variety of comprehensive chemical induction models that recapitulate the natural pathogenesis of acute liver injury. Their mechanism is always based on redox imbalance-induced direct hepatotoxicity and massive hepatocyte cell death, which can trigger immune cell activation and recruitment to the liver. However, the pathogenesis of these models has not been fully stated. Many studies showed that gut microbiota plays a crucial role in chemical-induced liver injury. Hepatotoxicity is likely induced by imbalanced microbiota homeostasis, gut mucosal barrier damage, systemic immune activation, microbial-associated molecular patterns, and bacterial metabolites. Meanwhile, many preclinical studies have shown that supplementation with probiotics can improve chemical-induced liver injury. In this review, we highlight the pathogenesis of gut microorganisms in chemical-induced acute liver injury animal models and explore the protective mechanism of exogenous microbial supplements on acute liver injury.

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“…Macrophages, an important part of innate immune system, are related to various diseases and play a vital role in sepsis by regulating immune responses and inflammatory factors secretion, such as tumor necrosis factor (TNF)-α, IL-10, and IFN-g [ 3 , 4 ]. Recent research has indicated that excessive production of inflammatory cytokines was observed during sepsis [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Sun

Meng

et al. 2020

Open Medicine

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In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis.

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Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

Cited by 25 publications

References 43 publications

Plasmacytoid dendritic cells protect against immune-mediated acute liver injury via IL-35

Plasmacytoid dendritic cells protect against immune-mediated acute liver injury via IL-35

Gut Microbiota and Chemical-Induced Acute Liver Injury

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

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