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Background: Oral lichen planus (OLP) is a common oral mucosal disease, clinically categorized into erosive OLP (EOLP) and non-erosive OLP (NEOLP) based on symptoms, but its pathogenic mechanism remains unclear. This study aims to explore the relationship between OLP and the oral microbiome. Methods: We collected oral mucosal samples from 49 patients and 10 healthy individuals and conducted 16S rRNA and ITS gene sequencing to explore the oral fungal and bacterial communities. Results: We observed significantly lower α diversity of fungi in the EOLP group, with Candida being significantly enriched as the main dominant genus. In the NEOLP group, Aspergillaceae were significantly enriched. The EOLP group showed significant enrichment of Aggregatibacter and Lactobacillus, but the relative abundance of Streptococcus was notably lower than in the other two groups. In the NEOLP group, two species including Prevotella intermedia were significantly enriched. The microbial co-occurrence and co-exclusion networks display distinct characteristics across the three groups, with Lactobacillus assuming a significant bridging role in the ELOP group. Conclusions: Our study indicates that EOLP and NEOLP experience varying degrees of dysbiosis at both the fungal and bacterial levels. Therefore, the pathogenic mechanisms and interactive relationships of these microbiota associated with OLP merit further in-depth investigation.
The microbial community in the oral lesions of EOLP patients exhibits highly distinctive features, both in terms of bacteria and fungi.In NEOLP patients, the overall bacterial composition does not exhibit significant differences compared to the healthy population, but P. intermedia and Aspergillaceae are notably enriched.
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BACKGROUND: Alterations in the intestinal microbiota may play a role in the pathogenesis of functional bowel disorders (FBDs). Probiotics are widely used to improve intestinal dysbacteriosis in FBDs. In the context of FBDs, washed microbiota transplantation (WMT) appear to be a promising therapeutic option. We aimed to compare probiotics with WMT by using a propensity-score matching analysis (PSMA). METHODS: We conducted a retrospective investigation of 103 patients with FBDs, including irritable bowel syndrome (IBS), functional constipation (FC), functional diarrhea (FDr), functional abdominal bloating (FAB). Patients were divided into the WMT group or probiotics group (taking probiotics capsules). Data on the following parameters were matched for PSMA: age; sex; disease course; body mass index; anxiety; insomnia; tobacco smoking; alcohol consumption; and levels of D-lactate, diamine oxidase, and lipopolysaccharide. Intestinal barrier function (IBF) and symptoms were evaluated both before and after treatment initiation. Prognostic factors were assessed by Cox proportional hazards regression analysis. RESULTS: PSMA identified in 34 matched pairs (11 IBS, 12 FC, 7 FDr, and 4 FAB in the probiotics group and 14 IBS, 13 FC, 5 FDr, and 2 FAB in the WMT group. Improvement of FBD symptoms was greater with WMT than probiotics (P = 0.002). The WMT group had significantly fewer patients with intestinal barrier damage than the probiotics group (38.2% vs. 67.6%, P = 0.041). This improvement of FBD with WMT was further reflected as a reduction in D-lactate levels (P = 0.031). Increased D-lactate levels which were identified as a prognostic factor for FBDs (HR = 0.248, 95%CI 0.093-0.666, P = 0.006) in multivariate Cox regression analysis. CONCLUSION: WMT could improve symptoms and IBF in patients with FBDs. Increased D-lactate levels in patients with FBDs may predict a favorable response to WMT treatment.
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Gastroenteropatias , Microbioma Gastrointestinal , Síndrome do Intestino Irritável , Humanos , Função da Barreira Intestinal , Estudos Retrospectivos , Flatulência , LactatosRESUMO
The highly virulent and antigenic variant of Pseudorabies virus (PRV) that emerged from classical Bartha-K61-vaccinated pig herds has caused substantial economic losses to the swine industry in China since 2011. A safe and more effective vaccine is most desirable. In this study, a gE/TK gene-deficient PRV, namely, HD/c, was constructed based on a PRV type II DX strain isolated from a commercial vaccine-immunized farm and the HD/c-based inactivated vaccine was formulated and evaluated for its safety, immunogenicity, and protective efficacy in mice and piglets. The resulting PRV HD/c strain has a similar growth curve to the parental DX strain. After vaccination, the inactivated HD/c vaccine did not cause any visible gross pathological or histopathological changes in the tissues of mice and piglets and provided rapid and potent protection against the challenge of the classical and variant PRVs at day 21 post-vaccination in mice. A single immunization of 108.5TCID50 inactivated PRV HD/c strain-elicited robust immunity with high titer of neutralizing antibody and provided complete protection from the lethal challenge of PRV DX strain in piglets. These results indicated that the inactivated PRV HD/c vaccine with the deletion of gE/TK genes was a safe and effective PRV vaccine candidate for the control of PRV.
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As a member of the nuclear receptor superfamily, the pregnane X receptor (PXR) is a ligand-activated transcription factor. PXR is highly expressed in liver and intestinal tissues, and also found in other tissues and organs, such as stomach and kidney. After heterodimerization with retinoid X receptor (RXR), PXR recruits numerous co-activating factors, and binds to specific DNA response elements to perform transcriptional regulation of the downstream target genes. As an acknowledged receptor for xenobiotics, PXR was initially considered as a nuclear receptor regulating drug metabolizing enzymes and transporters. However, nowadays, PXR has also been recognized as an important endobiotic receptor. Recent studies have shown that PXR activation can regulate glucose metabolism, lipid metabolism, steroid endocrine homeostasis, detoxification of cholic acid and bilirubin, bone mineral balance, and immune inflammation in vivo. This review focuses on the role of PXR in metabolism of endogenous substances.
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Animais , Humanos , Regulação da Expressão Gênica , Receptor de Pregnano X , Metabolismo , Xenobióticos , MetabolismoRESUMO
Objective To explore effects of application of home care mobile app for management of discharged patients with permanent enterostomy.Methods The home care mobile app was designed and developed.Totally 100 patients with permanent enterostomy from 15 tertiary hospitals in Jiangsu Province were provided with mobile home care intervention,and effects of the app were evaluated.Results Six months after discharge,the DET score of patients who used the app was 0.47±1.55 and was lower than those who did not use the app 1.16±3.01.Meanwhile 83％ of the patients could complete stoma self-care through the platform without going to the hospital,and 98.0％ of the patients were satisfied with the home care service platform.Conclusion The home care mobile app can improve skin problem around the stoma,and ensure the continuity of nursing after discharge.
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AIM:To explore the effects of chloroquine (CQ) on collagen Ⅰ and collagen Ⅲ expression in activated rat hepatic stellate cell line HSC-T6 and the possible mechanism.METHODS:Transforming growth factor-β1 (TGF-β1) was used to activate HSC-T6 cells and 3 doses of CQ was administered for 24 h.The cells were divided into 5 groups as follows:control group,TGF-β1 group,TGF-β1 + CQ (15 μmol/L) group,TGF-β1 + CQ (30 μ mol/L) group and TGF-β1 + CQ (60 μmol/L) group.Western blot was used to determine the expression of LC3-Ⅱ/LC3-Ⅰ,P62 and o-SMA in activated HSC-T6 cells.The expression of collagen Ⅰ and collagen Ⅲ was detected by immunocytochemical staining,Western blot and RT-qPCR.Western blot and RT-qPCR were also used to detect the expression of matrix metalloproteinase-13 (MMP-13),tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 at mRNA and protein levels.RESULTS:The ratio of LC3-Ⅱ / LC3-Ⅰ and P62 expression were increased after CQ intervention.Moreover,they were significantly higher in the TGF-β1 + CQ groups than those in TGF-β1 group (P ＜ 0.01).The expression of collagen Ⅰ and collagen Ⅲ at mRNA and protein levels was significantly increased in all TGF-β1 + CQ groups as compared with TGF-β1 group (P ＜0.01),and it was markedly increased among TGF-β1 + CQ groups in a dose-dependent manner.The expression of MMP-13 at mRNA and protein levels was significantly lowered and that of TIMP-1 and TIMP-2 was significantly increased in TGF-β1 + CQ groups as compared with TGF-β1 group (P ＜0.05).CONCLUSION:Inhibition of autophagy by CQ in activated HSC-T6 cells up-regulates the expression of collagen Ⅰ and collagen Ⅲ in a dose-dependent way,probably due to reduction of MMP-13 and enhancement of TIMP-1 and TIMP-2 expression.
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AIM:To explore the effects of chloroquine (CQ) on collagen Ⅰ and collagen Ⅲ expression in activated rat hepatic stellate cell line HSC-T6 and the possible mechanism.METHODS:Transforming growth factor-β1 (TGF-β1) was used to activate HSC-T6 cells and 3 doses of CQ was administered for 24 h.The cells were divided into 5 groups as follows:control group,TGF-β1 group,TGF-β1 + CQ (15 μmol/L) group,TGF-β1 + CQ (30 μ mol/L) group and TGF-β1 + CQ (60 μmol/L) group.Western blot was used to determine the expression of LC3-Ⅱ/LC3-Ⅰ,P62 and o-SMA in activated HSC-T6 cells.The expression of collagen Ⅰ and collagen Ⅲ was detected by immunocytochemical staining,Western blot and RT-qPCR.Western blot and RT-qPCR were also used to detect the expression of matrix metalloproteinase-13 (MMP-13),tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 at mRNA and protein levels.RESULTS:The ratio of LC3-Ⅱ / LC3-Ⅰ and P62 expression were increased after CQ intervention.Moreover,they were significantly higher in the TGF-β1 + CQ groups than those in TGF-β1 group (P ＜ 0.01).The expression of collagen Ⅰ and collagen Ⅲ at mRNA and protein levels was significantly increased in all TGF-β1 + CQ groups as compared with TGF-β1 group (P ＜0.01),and it was markedly increased among TGF-β1 + CQ groups in a dose-dependent manner.The expression of MMP-13 at mRNA and protein levels was significantly lowered and that of TIMP-1 and TIMP-2 was significantly increased in TGF-β1 + CQ groups as compared with TGF-β1 group (P ＜0.05).CONCLUSION:Inhibition of autophagy by CQ in activated HSC-T6 cells up-regulates the expression of collagen Ⅰ and collagen Ⅲ in a dose-dependent way,probably due to reduction of MMP-13 and enhancement of TIMP-1 and TIMP-2 expression.
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Objective: To investigate the role of extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathway in the pathogenesis of stress-induced gastric ulcer. Methods: Animal model of stress-induced gastric ulcer was established in rats with water-immersion restraint (WIR) stress. The mucosal activation of ERK1/2 was observed before and 5, 15 and 30 min, and 1, 2 and 3.5 h after WIR stress. Some animals were also treated with an intravenous injection of PD98059 (1 mg/kg), a specific ERK1/2 inhibitor, 1 h prior to WIR stress. Expression of total ERK1/2 and caspase-3 were detected by Western blot analysis; ERK1/2 activity was measured by kinase activity assay using myelin basic protein as a specific substrate. DNA-binding activities of the transcription factors activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) were determined by electrophoretic mobility shift assays (EMSA). Mucosal TNF-α and IL-1β mRNA expression was analyzed by Northern blot analysis. The degrees of the gastric mucosal lesions were expressed as ulcer index (UI) and pathological evaluation. Apoptosis in the gastric mucosa was examined by an in situ TdT-mediated dUTP nick-end labeling (TUNEL) method. Results: Activated ERK1/2 was very weakly expressed in the gastric mucosa of normal rats. ERK1/2 was rapidly activated in the gastric mucosa of rats 15 min after WIR stress and the activity reached the maximal after 3.5 h. Pretreatment with PD98059 significantly inhibited ERK1/2 activation, decreased AP-1 and NF-κB activities and TNF-α and IL-β mRNA expression, and obviously relieved gastric mucosal lesions, accompanied by caspase-3 activation and increased apoptosis. Conclusion: The present results indicate that ERK1/2 activation plays an important role in the development of stress-induced gastric ulcer.
