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Gastric reactive hyperplasia (RH) is a common benign lesion of the gastric mucosa that can be resolved by conservative treatment without endoscopic intervention. Some RH lesions are indistinguishable from low-grade intraepithelial neoplasia (LGIN) lesions of gastric mucosa under endoscopy. The aim of this study was to investigate the morphological features of RH lesions under magnifying endoscopy combined with narrow-band imaging (ME-NBI). A retrospective study of 653 patients with superficial suspicious lesions of gastric mucosa was performed. According to the pathological results of biopsies, the final included lesions were divided into the RH group (n = 88) and LGIN group (n = 138). We analysed the microvascular and microsurface patterns of these lesions under ME-NBI, extracted the most significant combination of endoscopic features of RH lesions, and evaluated their diagnostic performance. ME-NBI characteristics that could distinguish RH lesions from LGIN lesions after univariate analysis were included in multivariate logistic regression. The results showed that ten characteristics, including intervening part (IP) length homogeneity, type III gastric pit pattern and homogeneity of marginal crypt epithelium (MCE), were statistically significant. Receiver operating characteristic (ROC) analysis showed that the triad of these features was the best combination for diagnosing RH lesions with an AUC of 0.886 (95% confidence interval; 0.842–0.929), the sensitivity of 85.5% and specificity of 79.5%. The triad of IP length homogeneity, type III pit pattern and MCE homogeneity under ME-NBI helps endoscopists to identify gastric RH lesions, thereby avoiding unnecessary biopsy and repeat endoscopy due to misjudgment of neoplastic lesions. [ABSTRACT FROM AUTHOR]

Narrow-band imaging (NBI) with magnifying endoscopy revealed a papillary-shaped microsurface and irregular microvessels in the lesion with clear demarcation (Fig. 17224936-f72ad495.mp4 Histologically, the tumor glands presented papillary or tubular growth with obvious structural atypia, and the tumor cell density was significantly increased (Fig. 4 a Histological examination showed tumor glands presented papillary or tubular growth with obvious structural atypia. b The tumor cell density was significantly increased. [Extracted from the article]

Cholesterol gallstone (CG) disease has relationships with several metabolic abnormalities. Astragalus polysaccharides (APS) have been shown to have multiple benefits against metabolic disorders. We attempted to uncover the effect and mechanism of action of APS on diet-induced CG formation in mice. Animals were fed a chow diet or lithogenic diet (LD) with or without APS supplementation. The effect of APS on CG formation was evaluated. The level of individual bile acids (BAs) in gallbladder bile and ileum were measured by liquid chromatography-tandem mass spectrometry. Real-time reverse transcription-quantitative polymerase chain reaction and western blotting were used to assess expression of the genes involved in BA metabolism and the enterohepatic circulation. Cecal contents were collected to characterize microbiota profiles. APS ameliorated LD-induced CG formation in mice. APS reduced the level of total cholesterol, bile acid hydrophobicity index and cholesterol saturation index in gallbladder bile. The protective effect of APS might result from reduced absorption of cholic acid in the intestine and increased hepatic BA synthesis. APS relieved the LD-induced activation of the intestinal farnesoid X receptor and decreased ileal expression of fibroblast growth factor 15. In the liver, expression of cytochrome P450 (Cyp) enzyme Cyp7a1 and Cyp7b1 was increased, whereas expression of adenosine triphosphate-binding cassette (Abc) transporters Abcg5 and Abcg8 was decreased by APS. APS improved the diversity of the gut microbiota and increased the relative abundance of the Bacteroidetes phylum. APS had demonstratable benefits against CG disease, which might be associated with enhanced BA synthesis and improved gut microbiota. Our results suggest that APS may be a potential strategy for the prevention of CG disease. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to evaluate the effect and related mechanisms of Mesenchymal stem cells (MSCs) and Angiotensin converting enzyme II (ACE II) on acute lung injury (ALI). Methods: MSCs were separated from umbilical cord cells, and the changes of phenotype before and after ACE II silence were observed using Flow Cytometer. ALI model was induced by 10 mg/mL bleomycin in 60 Balb/c mice, and the rest 8 mice were regarded as the baseline group. The mice were randomly divided into four groups ( n = 15): control, ACE II, stem, and stem + ACE II. The apoptotic index (AI) was calculated using TUNEL, and the detection of protein and mRNA of Bax, Bak and p53, Bcl-2, Grp78, CHOP and Caspase 12 were used by western-blot and RT-PCR, respectively. Results: The umbilical cord cells differentiated into stable MSCs about 14 days, and ACE II transfection reached a peak at the 5th day after transfection. ACE II silence did not affect the phenotype of MSCs. All the proteins and mRNAs expression except Bcl-2 in the stem and stem + ACE II were significantly lower than those in control from 8 h ( p < 0.05, p < 0.01), while Bcl-2 exhibited an opposite trend. Stem + ACE II performed a better effect than single stem in most indexes, including AI ( p < 0.05, p < 0.01). Conclusions: The co-administration of MSCs and ACE II can significantly suppress apoptosis in ALI mice, and may be an effective clinical treatment for ALI. [ABSTRACT FROM AUTHOR]

Abstract: The efficiencies of IFN-α based therapy in chronic genotype 1b HCV patients are still unsatisfied to date. The mechanisms underlining treatment failure remain unclear and controversial. To investigate HCV sequence evolution in unsuccessfully treated genotype 1b patients before, during and after the therapy, full-length open-reading-frame of HCV genomes at week 0, week 48 and year 5 in one breakthrough and one nonresponse patients were amplified by reverse transcription (RT)-nested-PCR and sequenced. Mutations were scored and analyzed according to their locations in the HCV genome. HCV sequences in the breakthrough patient displayed significantly more mutations during the one-year therapy than that in the nonresponse patient, with p7 and NS2 encoding regions having the highest mutation rates. Most of the mutations selected during the therapy phase in the breakthrough patient were maintained and few new mutations arose in the four-year post-therapy phase, suggesting these mutations might not compromise viral fitness. Altogether our data suggest that mutations occurred during the therapy phase in the breakthrough patient are likely driven by the action of interferon and ribavirin, and these mutations may have important effects on the responses to interferon based therapy in genotype 1b HCV patients. [Copyright &y& Elsevier]

Cholesterol overloading and bile acid metabolic disorders play an important role in the onset of cholesterol gallstone (CGS). Short-chain fatty acids (SCFAs) can regulate bile acid metabolism by modulating the gut microbiota. However, the role and mechanism by which sodium butyrate (NaB) targets bile acids to attenuate CGS are still unknown. In this study, continuous administration of 12 mg/day for 8 weeks was decreased the incidence of gallstones induced by lithogenic diet (LD) from 100% to 25%. NaB modulated SCFAs and improved the gut microbiota. The remodeling of the gut microbiota changed the bile acid compositions and decreased cecal tauro-α-muricholic acid (T-α-MCA) and tauro-β-muricholic acid (T-β-MCA) which are effective farnesoid X receptor (FXR) antagonists. The quantitative real-time PCR examination showed that NaB significantly increased levels of ileal Fxr, fibroblast growth factor-15 (Fgf-15) and small heterodimer partner (Shp) mRNA and subsequently inhibited bile acid synthesis. In addition, NaB enhanced bile acid excretion by increasing the levels of hepatic multidrug resistance protein 2 (Mdr2) and bile salt export pump (Bsep) mRNA, and it enhanced bile acid reabsorption in the intestine by increasing the levels of ileal bile acid transporter (Ibat) mRNA. In addition, NaB reduced the absorption of cholesterol in the intestine and inhibited the excretion of cholesterol in the liver, which reduced the cholesterol concentration in serum and bile. Furthermore, the protective effects of NaB administration were abolished by FXR antagonists. Taken together, our results suggest that NaB mitigates CGS by modulating the gut microbiota to regulate the FXR-FGF-15/SHP signaling pathway. [ABSTRACT FROM AUTHOR]

Introduction: Patients with liver cancer are susceptible to experiencing a decline in muscle mass and function, which can lead to physical frailty and have a negative impact on prognosis. However, there is currently a lack of physical activity interventions specifically tailored for these patients. Therefore, we have developed a modular multimodal hospital-home chain physical activity rehabilitation programme (3M2H-PARP) designed specifically for patients with liver cancer undergoing transarterial chemoembolisation (TACE). We aim to validate the effectiveness and feasibility of this programme through a randomised controlled trial (RCT)., Methods and Analysis: 3M2H-PARP RCT will compare a 12-week, modular, multimodal physical activity rehabilitation programme that includes supervised exercise in a hospital setting and self-management exercise at home. The programmes consist of aerobic, resistance, flexibility and balance exercise modules, and standard survivorship care in a cohort of liver cancer survivors who have undergone TACE. The control group will receive standard care. A total of 152 participants will be randomly assigned to either the 3M2H-PARP group or the control group. Assessments will be conducted at three time points: baseline, after completing the intervention and a 24-week follow-up visit. The following variables will be evaluated: liver frailty index, Functional Assessment of Cancer Therapy-Hepatobiliary subscale, Cancer Fatigue Scale, Pittsburgh Sleep Quality Index, Hospital Anxiety and Depression Scale and physical activity level. After the completion of the training programme, semi-structured interviews will be conducted with participants from the 3M2H-PARP group to investigate the programme's impact on their overall well-being. SPSS V.26.0 software will be used for statistical analyses., Ethics and Dissemination: Ethical approval has been granted by the Jiangnan University School of Medicine Research Ethics Committee. The findings will be disseminated through publication in a peer-reviewed journal., Trial Registration Number: ChiCTR2300076800., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Competing Interests: The authors declare that they have no conflict of interest.

Background: Endoscopically visible gastric neoplastic lesions (GNLs), including early gastric cancer and intraepithelial neoplasia, should be accurately diagnosed and promptly treated. However, a high rate of missed diagnosis of GNLs contributes to the potential risk of the progression of gastric cancer. The aim of this study was to develop a deep learning-based computer-aided diagnosis (CAD) system for the diagnosis and segmentation of GNLs under magnifying endoscopy with narrow-band imaging (ME-NBI) in patients with suspected superficial lesions., Methods: ME-NBI images of patients with GNLs in two centers were retrospectively analysed. Two convolutional neural network (CNN) modules were developed and trained on these images. CNN1 was trained to diagnose GNLs, and CNN2 was trained for segmentation. An additional internal test set and an external test set from another center were used to evaluate the diagnosis and segmentation performance., Results: CNN1 showed a diagnostic performance with an accuracy, sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of 90.8%, 92.5%, 89.0%, 89.4% and 92.2%, respectively, and an area under the curve (AUC) of 0.928 in the internal test set. With CNN1 assistance, all endoscopists had a higher accuracy than for an independent diagnosis. The average intersection over union (IOU) between CNN2 and the ground truth was 0.5837, with a precision, recall and the Dice coefficient of 0.776, 0.983 and 0.867, respectively., Conclusions: This CAD system can be used as an auxiliary tool to diagnose and segment GNLs, assisting endoscopists in more accurately diagnosing GNLs and delineating their extent to improve the positive rate of lesion biopsy and ensure the integrity of endoscopic resection., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Liu, Dong, Cheng, Bu, Qiu, Yang, Wang, Niu, Wu, Xu, Mao, Lu, Wan and Zhou.)

Cholesterol gallstone (CGS) disease is characterized by an imbalance in bile acid (BA) metabolism and is closely associated with gut microbiota disorders. However, the role and mechanism by which probiotics targeting the gut microbiota attenuate cholesterol gallstones are still unknown. In this study, Limosilactobacillus reuteri strain CGMCC 17942 and Lactiplantibacillus plantarum strain CGMCC 14407 were individually administered to lithogenic-diet (LD)-fed mice for 8 weeks. Both Lactobacillus strains significantly reduced LD-induced gallstones, hepatic steatosis, and hyperlipidemia. These strains modulated BA profiles in the serum and liver, which may be responsible for the activation of farnesoid X receptor (FXR). At the molecular level, L. reuteri and L. plantarum increased ileal fibroblast growth factor 15 (FGF15) and hepatic fibroblast growth factor receptor 4 (FGFR4) and small heterodimer partner (SHP). Subsequently, hepatic cholesterol 7α-hydroxylase (CYP7A1) and oxysterol 7α-hydroxylase (CYP7B1) were inhibited. Moreover, the two strains enhanced BA transport by increasing the levels of hepatic multidrug resistance-associated protein homologs 3 and 4 (Mrp3/4), hepatic multidrug resistance protein 2 (Mdr2), and the bile salt export pump (BSEP). In addition, both L. reuteri and L. plantarum reduced LD-associated gut microbiota dysbiosis. L. reuteri increased the relative abundance of Muribaculaceae , while L. plantarum increased that of Akkermansia. The changed gut microbiota was significantly negatively correlated with the incidence of cholesterol gallstones and the FXR-antagonistic BAs in the liver and serum and with the FXR signaling pathways. Furthermore, the protective effects of the two strains were abolished by both global and intestine-specific FXR antagonists. These findings suggest that Lactobacillus might relieve CGS through the FXR signaling pathways. IMPORTANCE Cholesterol gallstone (CGS) disease is prevalent worldwide. None of the medical options for prevention and treatment of CGS disease are recommended, and surgical management has a high rate of recurrence. It has been reported that the factors involved in metabolic syndrome are highly connected with CGS formation. While remodeling of dysbiosis of the gut microbiome during improvement of metabolic syndrome has been well studied, less is known about prevention of CGS formation after regulating the gut microbiome. We used the lithogenic diet (LD) to induce an experimental CGS model in C57BL/6J mice to investigate protection against CGS formation by Limosilactobacillus reuteri strain CGMCC 17942 and Lactiplantibacillus plantarum strain CGMCC 14407. We found that these L. reuteri and L. plantarum strains altered the bile acid composition in mice and improved the dysbiosis of the gut microbiome. These two Lactobacillus strains prevented CGS formation by fully activating the hepatic and ileal FXR signaling pathways. They could be a promising therapeutic strategy for treating CGS or preventing its recurrence.

Gypenosides (GPs), obtained from Gynostemma pentaphyllum (Thunb.) Makino, have been traditionally prescribed to treat metabolic disorders in Asians. This study assessed whether GPs could prevent lithogenic diet (LD)-induced cholesterol gallstone (CG) formation and enhance CG dissolution in mice. Gallstone-susceptible C57BL/6J mice were fed an LD or normal chow, with or without GPs. Bile acids (BAs) in gallbladder bile were analyzed by liquid chromatography-tandem mass spectrometry. Differentially expressed hepatic genes were identified by RNA sequencing, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. GPs were found to prevent LD-induced CG formation and to dissolve pre-existing LD-induced CGs. GPs reduced total cholesterol levels and increased BA levels in bile, as well as reducing the BA Hydrophobicity Index, ratio of 12α-hydroxylated (12α-OH) to non-12α-OH BAs, and Cholesterol Saturation Index in gallbladder bile. GO and KEGG pathway enrichment analyses indicated that GPs-induced genes were involved in BA biosynthesis and cholesterol metabolism. GPs increased the hepatic expression of genes encoding the cytochrome P450 (Cyp) enzymes Cyp7a1, Cyp7b1, and Cyp8b1, while decreasing the hepatic expression of genes encoding the adenosine triphosphate-binding cassette (Abc) transporters Abcg5 and Abcg8. GPs may be a promising strategy for preventing and dissolving CGs., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zhuang, Cheng, Xia, Ning, Wu, Shen, Shi, Huang, Dong and Wan.)

Background: A root cause analysis (RCA) is a structured method used to address problems. It seeks to identify the root causes of problems, and proposes solutions to achieve an ultimate goal. This study sought to investigate the effects of an RCA in treating elderly patients with acute pancreatitis (AP)., Methods: 94 patients with AP, who had been admitted to our hospital from January 2019 to January 2020, were enrolled in the study. The patients were divided into two groups using the random number table method. Each group comprised 47 patients. The control group received routine care, while the observation group underwent RCA care. The clinical efficacy, patients' negative emotions before and after the intervention, the incidence of complications, and patients' levels of satisfaction with the nursing they received were compared between the two groups., Results: The total clinical effective rate of the observation group was higher than that of the control group (P<0.05). The Hamilton Anxiety Scale and Hamilton Depression Scale scores of the observation group were lower than those of the control group after the 2-week intervention (P<0.05). The incidence of total complications in the observation group was lower than that in the control group (P<0.05). The observation group's level of satisfaction with the nursing they received was higher than that of the control group (P<0.05)., Conclusions: The RCA method can improve clinical efficacy, relieve negative emotion, reduce the incidence of complications, and improve the level of satisfaction with nursing of elderly patients with AP. It is worthy of promotion., Trial Registration: Chinese Clinical Trial Registry ChiCTR2100045908.

Adiponectin, an adipose-derived adipokine, possesses a hepatoprotective role in various liver disorders. It has been reported that hypoadiponectinemia can affect with the progression of non-alcoholic fatty liver diseases (NAFLD). Inflammasome activation has been recognized to play a major role during the progression of NAFLD. This research aimed to explore the effect of adiponectin on palmitate (PA)-mediated NLRP3 inflammasome activation and its potential molecular mechanisms. Male adiponectin-knockout (adiponectin-KO) mice and C57BL/6 (wild-type) mice were fed a high-fat-diet (HFD) for 12 weeks as an in vivo model of non-alcoholic steatohepatitis (NASH). Serum biochemical markers, liver histology and inflammasome-related gene and protein expression were determined. In addition, the hepatocytes isolated from wide type mice were exposed to PA in the absence or presence of adiponectin and/or AMPK inhibitor. The activation of NLRP3 inflammasome was assessed by mRNA and protein expression. Furthermore, ROS production and related signaling pathways were also evaluated. In the in vivo experiments, excessive hepatic steatosis with increased NLRP3 inflammasome and its complex expression were found in adiponectin-KO mice compared to wild-type mice. Moreover, the expression levels of NLRP3 inflammasome pathway molecules (NFκB and ROS) were upregulated, while the phosphorylation levels of AMPK, JNK, and Erk1/2 were downregulated in adiponectin-KO mice compared with wild-type mice. In the in vitro study, PA increased lipid droplet deposition, NF-kB signaling and ROS production. Additionally, PA significantly promoted NLRP3 inflammasome activation and complex gene and protein expression in hepatocytes. Adiponectin could abolish PA-mediated inflammasome activation and decrease ROS production, which was reversed by AMPK inhibitor (compound C). Furthermore, the results showed that the inhibitory effect of adiponectin on PA-mediated inflammasome activation was regulated by AMPK-JNK/ErK1/2-NFκB/ROS signaling pathway. Adiponectin inhibited PA-mediated NLRP3 inflammasome activation in hepatocytes. Adiponectin analogs or AMPK agonists could serve as a potential novel agent for preventing or delaying the progression of NASH and NAFLD., (Copyright © 2020 Dong, Zhuang, Ye, Ning, Wu, Lu and Wan.)

Background: Colon cancer is the most common malignant tumor of the gastrointestinal tract. This cancer and the related treatments bring a raft of lasting physiological and psychological impacts to patients. This study explored the effects of attention and interpretation therapy (AIT) on improving psychological resilience, cancer-related fatigue (CRF), and negative emotions in patients after colon cancer surgery., Methods: Patients who had undergone colon cancer surgery in the Affiliated Hospital of Jiangnan University were selected and randomly allocated into an experimental group and a control group, each with 100 cases. Patients in the control group received routine intervention measures, while the experimental group received an extra 10 weeks of AIT. Before and after 10 weeks of intervention, the effects of intervention were evaluated using the Connor-Davidson Resilience Scale (CD-RISC), Self-Rating Anxiety Scale (SAS), Selfrating Depression Scale (SDS) and the Revised Piper Fatigue Scale (PFS-R)., Results: Before the intervention, there was no statistical difference between the scores of psychological resilience, CRF, and negative emotions between the two groups (P>0.05). We compared the scores before and after the 10 weeks of intervention and found that the scores of psychological resilience of the experimental group were higher than before, and the scores of CRF and negative emotion were lower than before. After the intervention, the psychological resilience score of the experimental group was higher than that of the control group, the CRF and negative emotions scores were lower than those of the control group, and the differences were statistically significant (P<0.05)., Conclusions: AIT can effectively strengthen the psychological resilience of patients after colon cancer surgery to a certain extent, reduce anxiety and depression, reduce the degree of CRF, and thus improve the patients' quality of life postoperatively.

Background: Pancreatic encephalopathy is the most serious complication of severe acute pancreatitis (SAP) and substantially increases mortality. Delirium is a common clinical manifestation of pancreatic encephalopathy. This study aimed to assess the clinical effects of an improved version of the Hospital Elderly Life Program (HELP) on preventing delirium in elderly patients with SAP., Methods: A total of 106 patients with SAP aged 70 years or older were randomly divided into an experimental group (53 cases) and a control group (53 cases). The experimental group was given 2 weeks of conventional nursing combined with the HELP regimen, while the control group was given 2 weeks of conventional nursing. Conventional nursing included disease care, geriatric syndrome care and observation of critically ill patients. The incidence of delirium, severity of delirium, self-care ability, cognitive function, length of hospital stay, and patient satisfaction were compared between the 2 groups before and after the intervention., Results: The incidence of delirium was 4.00% in the experimental group and 16.98% in the control group; the difference was statistically significant (P=0.033). After 2 weeks of intervention, the experimental group showed significantly better self-care ability and cognitive function, shorter hospital stay, and greater patient satisfaction than the control group (all P<0.05)., Conclusions: The improved HELP protocol for elderly patients with SAP can reduce the incidence and severity of delirium, improve self-care ability and cognitive function, shorten hospital stay, and increase patient satisfaction.

Background: The NLRP3 inflammasome activation plays an important role in the development of NASH and fibrogenesis. However, the mechanisms involved in NLRP3 activation in hepatic stellate cells (HSCs) have been unclear. The aim of this study was to investigate the mechanism of NLRP3 activation in HSCs and the role of NLPR3 inflammasome activation in HSCs on the development of nonalcoholic steatohepatitis (NASH) to fibrosis., Methods: Primary HSCs isolated from SD rats were incubated with palmitic acid and/or LPS, respectively. For in vivo animal experiment, 4-week-old SD rats were fed with high fat diet (HF-diet) for 12 weeks, SD rats were sacrificed at 0, 4, 8 and 12 w. In another group of animal experiment, 4-week-old SD rats were fed with HF-diet and a NLRP3 inhibitor (intraperitoneal injection of NLRP3 inhibitor glybenclamide 5 mg/kg, injected every 3 days) for 12 weeks. Liver tissue and serum were harvested. RT-PCR, WB, ELISA, immunofluorescence and immunohistochemistry were performed to assess the NLRP3 inflammasome activation and signal molecules., Results: Palmitic acid stimulated NLPR3 inflammasome activation and fibrotic phenotype change in primary HSCs, LPS sensitizes the response of HSCs to palmitic acid. TLR4-NF-κB signal pathway was involved in NLRP3 inflammasome activation in palmitic acid-exposed HSCs and HF diet-induced NASH. It is evident that administration of NLRP3 inhibitor reduced the development of NASH to liver fibrosis in the NASH rat model., Conclusions: Palmitic acid stimulates NLRP3 inflammasome activation through the TLR4-NF-κB signal pathway in HSCs. NLRP3 inflammasome activation in HSCs exacerbates the development of NASH to liver fibrosis., Competing Interests: Conflicts of Interest: The authors have no conflicts of interest to declare., (2020 Annals of Translational Medicine. All rights reserved.)

Chronic hepatitis B (CHB) virus infection is caused by compromised host immunity, but the precise underlying mechanism remains unclear. Retinoic acid-inducible gene I (RIG-I) triggers antiviral immunity by inducing interferon-β (IFN-β) production following viral infection. To investigate the role of the RIG-I-IFN-β signaling pathway in monocyte-derived dendritic cells (moDCs) during CHB infection, moDCs were generated by stimulating CD14+ monocytes in vitro. MoDCs from patients with CHB, acute hepatitis B (AHB) and healthy controls (HCs) were challenged with vesicular stomatitis virus (VSV) and the levels of RIG-I, IFN-β promoter stimulator 1 (IPS-1) and IFN-β in the stimulated moDCs were determined. Following 16 h of VSV stimulation, RIG-I expression was reduced by 50% in moDCs from CHB patients and by 70% in moDCs from AHB patients relative to HC moDCs, concomitant with a 20% decrease in IFN-β expression in CHB patients relative to AHB patients and HCs. Additionally, a significant correlation between the RIG-I/IPS-1 ratio and alanine aminotransferase (ALT) level was observed. To further investigate the function of RIG-I in chronic hepatitis B virus (HBV) infection, HepG2 or HepG2.2.15 (HBV-transformed) cell lines were challenged with VSV following RIG-1 transfection. IFN-β induction was suppressed in HepG2.2.15 cells, but was restored following RIG-I transfection. Taken together, these data indicate that compromised moDC function in CHB patients is attributable to an impaired RIG-I-IFN-β signaling pathway, which results in compromised host viral clearance and HBV persistence in a susceptible population.