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The developmental changes in intestinal epithelial cell proliferation,differentiation,and shedding in weaning piglets

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Animal Nutrition 2022年第2期9卷 214-222页

作者： Min Wang Lixia Wang Xian Tan Lei Wang Xia Xiong Yancan Wang Qiye Wang Huansheng Yang Yulong Yin Hunan International Joint Laboratory of Animal intestinal Ecology and Health Laboratory of Animal Nutrition and Human HealthCollege of Life SciencesHunan Normal UniversityChangsha 410081HunanChina Hunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic Process Hunan Provincial Engineering Research Center for Healthy Livestock and Poultry ProductionKey Laboratory of Agro-ecological Processes in Subtropical RegionInstitute of Subtropical AgricultureChinese Academy of SciencesChangsha 410125HunanChina

intestinal epithelial homeostasis plays an important role in intestinal morphology and function.However,the developmental changes in intestinal epithelial cell turnover in piglets during early weaning are unknown so far.Thus,the aim of this work was to detect changes in piglet gut development from weaning to post-weaning d 14.Accordingly,40 piglets were used in the present study,and 8 piglets were randomly selected for sampling at d 0,1,3,7 and 14 post-weaning,respectively.The results showed that weaning stress significantly affected small intestinal morphological architecture,and this impact was the worst on d 3,and then returned to normal on d 14.Furthermore,the number of the marker of proliferation Ki-67(Ki67)positive cells was decreased on d 1 and 3,and then recovered on d 14(Pepithelial cell shedding on d 1 to 7 compared on d 0(Pintestinal enterocytes,goblets and endocrine cells(Pintestinal epithelial cell proliferation,differentiation and shedding,and the mTOR signaling pathway was involved in this process.Our findings provide a cellular mechanism for intestinal developmental changes during weaning periods.This may provide nutritionists with better insight into designing efficient in-feed alternatives for preventing the unfavorable gut development in weaning piglets.

关键词： intestinal epithelial cell Proliferation Differentiation Shedding Weaning piglet

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Qingyi decoction attenuates intestinal epithelial cell injury via the calcineurin/nuclear factor of activated T-cells pathway

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World Journal of Gastroenterology 2022年第29期28卷 3825-3837页

作者： Guan-Yu Wang Dong Shang Gui-Xin Zhang Hui-Yi Song Nan Jiang Huan-Huan Liu Hai-Long Chen Department of General Surgery The First Affiliated Hospital of Dalian Medical UniversityDalian 116011Liaoning ProvinceChina Institute of Integrative Medicine of Dalian Medical University Dalian 116044Liaoning ProvinceChina Laboratory of Integrative Medicine The First Affiliated Hospital of Dalian Medical UniversityDalian 116011Liaoning ProvinceChina

BACKGROUND Recent studies have demonstrated that dysfunction of the intestinal barrier is a significant contributing factor to the development of severe acute pancreatitis(SAP).A stable intestinal mucosa barrier functions as a major anatomic and functional barrier,owing to the balance between intestinal epithelial cell(IEC)proliferation and apoptosis.There is some evidence that calcium overload may trigger IEC apoptosis and that calcineurin(CaN)/nuclear factor of activated Tcells(NFAT)signaling might play an important role in calcium-mediated apoptosis.AIM To investigate the potential mechanisms underlying the therapeutic effect of Qingyi decoction(QYD)in SAP.METHODS A rat model of SAP was created via retrograde infusion of sodium deoxycholate.Serum levels of amylase,tumor necrosis factor(TNF-α),interleukin(IL)-6,D-lactic acid,and diamine oxidase(DAO);histological changes;and apoptosis of IECs were examined in rats with or without QYD treatment.The expression of the two subunits of CaN and NFAT in intestinal tissue was measured via quantitative realtime polymerase chain reaction and western blotting.For in vitro studies,Caco-2 cells were treated with lipopolysaccharide(LPS)and QYD serum,and then cell viability and intracellular calcium levels were detected.RESULTS Retrograde infusion of sodium deoxycholate increased the severity of pancreatic and intestinal pathology and the levels of serum amylase,TNF-α,and IL-6.Both the indicators of intestinal mucosa damage(D-lactic acid and DAO)and the levels of IEC apoptosis were elevated in the SAP group.QYD treatment reduced the serum levels of amylase,TNF-α,IL-6,D-lactic acid,and DAO and attenuated the histological findings.IEC apoptosis associated with SAP was ameliorated under QYD treatment.In addition,the protein expression levels of the two subunits of CaN were remarkably elevated in the SAP group,and the NFATc3 gene was significantly upregulated at both the transcript and protein levels in the SAP group compared with the control group.QYD significantly restrained CaN

关键词： Severe acute pancreatitis intestinal epithelial cell Apoptosis Calcineurin/nuclear factor of activated T-cells pathway Qingyi decoction

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Anthrax lethal toxin and tumor necrosis factor-a synergize on intestinal epithelia to induce mouse death

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Protein & cell 2024年第2期15卷 135-148页

作者： Xinhe Gao Teng Teng Yifei Liu Tingting Ai Rui Zhao Yilong Fu Peipei Zhang Jiahuai Han Yingying Zhang State Key Laboratory of cellular Stress Biology School of Life SciencesFaculty of Medicine and Life SciencesXiamen UniversityXiamen 361102China Research Unit of cellular Stress of CAMS Xiang'an Hospital of Xiamen UniversityCancer Research Center of Xiamen UniversitySchool of MedicineFaculty of Medicine and Life SciencesXiamen UniversityXiamen 361102China Laboratory Animal Center Faculty of Medicine and Life SciencesXiamen UniversityXiamen 361102China

Bacillus anthracis lethal toxin(LT)is a determinant of lethal anthrax.Its function in myeloid cells is required for bacterial dissemination,and LT itself can directly trigger dysfunction of the cardiovascular system.The interplay between LT and the host responses is important in the pathogenesis,but our knowledge on this interplay remains limited.Tumor necrosis factor-a(TNF-a)is a pleiotropic pro-inflammatory cytokine induced by bacterial infections.Since LT accumulates and cytokines,predominantly TNF,amass during B.anthracis infection,co-treatment of TNF+LT in mice was used to mimic in vivo conditions for LT to function in inflamed hosts.Bone marrow transplantation and genetically engineered mice showed unexpectedly that the death of intestinal epithelial cells(IECs)rather than that of hematopoietic cells led to LT+TNF-induced lethality.Inhibition of p38a mitogen-activated protein kinase(MAPK)signaling by LT in IECs promoted TNF-induced apoptosis and necroptosis of IECs,leading to intestinal damage and mouse death.Consistently,p38a inhibition by LT enhanced TNF-mediated cell death in human colon epithelial HT-29 cells.As intestinal damage is one of the leading causes of lethality in anthrax patients,the IEC damage caused by LT+TNF would most likely be a mechanism underneath this clinical manifestation and could be a target for interventions.

关键词： lethal toxin TNF p38a intestinal epithelial cell cell death

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Adipose-derived mesenchymal stem cells alleviate TNBS-induced colitis in rats by influencing intestinal epithelial cell regeneration, Wnt signaling, and T cell immunity

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World Journal of Gastroenterology 2020年第26期26卷 3750-3766页

作者： Jian-Guo Gao Mo-Sang Yu Meng-Meng Zhang Xue-Wei Gu Yue Ren Xin-Xin Zhou Dong Chen Tian-Lian Yan You-Ming Li Xi Jin Department of Gastroenterology The First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina Department of Colorectal Surgery The First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina

BACKGROUND Conventional Crohn’s disease(CD)treatments are supportive rather than curative and have serious side effects.Adipose-derived mesenchymal stem cells(ADSCs)have been gradually applied to treat various diseases.The therapeutic effect and underlying mechanism of ADSCs on CD are still not clear.AIM To investigate the effect of ADSC administration on CD and explore the potential mechanisms.METHODS Wistar rats were administered with 2,4,6-trinitrobenzene sulfonic acid(TNBS)to establish a rat model of CD,followed by tail injections of green fluorescent protein(GFP)-modified ADSCs.Flow cytometry,qRT-PCR,and Western blot were used to detect changes in the Wnt signaling pathway,T cell subtypes,and their related cytokines.RESULTS The isolated cells showed the characteristics of ADSCs,including spindle-shaped morphology,high expression of CD29,CD44,and CD90,low expression of CD34 and CD45,and osteogenic/adipogenic ability.ADSC therapy markedly reduced disease activity index and ameliorated colitis severity in the TNBS-induced rat model of CD.Furthermore,serum anti-sacchromyces cerevisiae antibody and panti-neutrophil cytoplasmic antibody levels were significantly reduced in ADSCtreated rats.Mechanistically,the GFP-ADSCs were colocalized with intestinal epithelial cells(IECs)in the CD rat model.GFP-ADSC delivery significantly antagonized TNBS-induced increased canonical Wnt pathway expression,decreased noncanonical Wnt signaling pathway expression,and increased apoptosis rates and protein level of cleaved caspase-3 in rats.In addition,ADSCs attenuated TNBS-induced abnormal inflammatory cytokine production,disturbed T cell subtypes,and their related markers in rats.CONCLUSION Successfully isolated ADSCs show therapeutic effects in CD by regulating IEC proliferation,the Wnt signaling pathway,and T cell immunity.

关键词： Crohn’s disease Adipose-derived mesenchymal stem cell intestinal epithelial cell Wnt pathway T cell Inflammation

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Ubiquitin-specific protease 47 regulates intestinal inflammation through deubiquitination of TRAF6 in epithelial cells

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Science China(Life Sciences) 2022年第8期65卷 1624-1635页

作者： Hu Lei Li Yang Hanzhang Xu Zhengting Wang Xiangyun Li Meng Liu Yingli Wu Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Gastroenterology Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Deubiquitinates(DUBs) alter the stabilities, localizations or activities of substrates by removing their ubiquitin conjugates,which are closely related to the development of inflammatory response. Here, we show that ubiquitin-specific protease 47(USP47) prevents inflammation development in inflammatory bowel disease(IBD). Compared with wild-type mice, Usp47 knockout mice are more susceptible to dextran sodium sulfate(DSS)-induced acute and chronic colitis with higher inflammatory cytokines expression and severe intestinal tissue damage. Chimeric mouse experiments suggest that non-hematopoietic cells mainly contribute to the phenotype. And, DSS-induced colitis of the Usp47 knockout mice depends on commensal bacteria.Mechanistically, down-regulation of USP47 aggravates the activation of NF-κB signaling pathway by increasing the K63-linked poly-ubiquitination of tumor necrosis factor receptor-associated factor 6(TRAF6) in intestinal epithelial cells. Furthermore, the expression of USP47, negatively correlated with the degree of inflammation, is lower at colonic inflammatory lesions than that non-inflammatory sites from the intestine from ulcerative colitis(UC) and Crohn's disease(CD) patients. These data, taken together, indicate that USP47 regulates intestinal inflammation through de-ubiquitination of K63-linked poly-ubiquitination TRAF6 in intestinal epithelial cells.

关键词： ubiquitin-specific protease 47 TRAF6 intestinal epithelial cell inflammation inflammatory bowel disease

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Effect of Echinacea Polysaccharide on Secretion of IL-1αmRNA by IEC-6 Injured by LPS

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Agricultural Biotechnology 2016年第6期5卷 35-36,43页

作者： Yanying ZHANG Qiumei SHI Qinghui JIA Guisheng GAO Guangping GAO Xinhua SHAO Hebei Normal University of Science&Technology Hebei Province Key Laboratory of Preventive Veterinary MedicineChangli 066600China Xinhua Keji Veterinary Medicine Co. Ltd.of Hebei ProvinceLuancheng 051430China

[ Objective ] This study was conducted to investigate Echinacea polysaccharide （EPS） on expression of tumor necrosis factor （TNF） under injury of intestinal epithelial cells （IEC-6） by lipopolysaccharide （LPS）, so as to discuss the action mechanism of EPS to injured cells. [Method] Total DNA was extracted with TRIzon reagent, TNF-α mRNA was amplified, and the amplification products were subjected to agarose gel electrophoresis and imaging. [Result] 50 μg/ml EPS could partially inhibited the production of IL-α mRNA by IEC-6 under the stimulation of LPS, while the inhibition of 2（10 and 500 μg/ml EPS on the level of IL-1α mRNA gradually increased with the concentration increasing; and IEC-6 cells pretreated with 50,100,200 and 500 μg/ml EPS for 24 h and then stimulated by 10 μml IPS for 1 and 4 h were analyzed by RT-PCR method, and it was found that the expression of IL-α mRNA induced by LPS could be effectively inhibited by EPS, and the inhibition rate at 4 h was higher than that at 1 h. [ Conclusion] EPS could play its role of protecting intestinal mucosa by inhibiting the secretion of IL-1α mRNA by cells under the stimulation of LPS, and such inhibition effects of EPS had concentration dependency and time dependency.

关键词： Echinacea pelysaccharide Lipopelysaccharide intestinal epithelial cell Inhibition Protection IL-1αmRNA

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Effect of Dachengqi Tang(大承气汤)Granule on Proliferation ofintestinal epithelial cells in Rats with Experimentalintestinal Obstruction

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Chinese Journal of Integrated Traditional and Western Medicine 2003年第1期9卷 57-59页

作者：康毅林秀珍 Department of Pharmacology Tianjin Medical UniversityTianjin 300070

Objective: To study the effects of Dachengqi Tang (DCQT) granule on the proliferation of the intestinal epithelial cells in rats with experimental intestinal obstruction. Methods: Experimental intestinal obstruction models were established in rats and autoradiography with 3 H-TdR was used to determine 3H-TdR labeling counts of intestinal epithelial cells in rats. Results: DCQT granule had no effects on 3H-TdR labeling counts of intestinal epithelial cells in normal rats. DCQT granule obviously increases the rate of renovation in intestinal epithelial cells of the intestinal obstruction rats. Conclusion: DCQT granule could reinforce the intestinal mucosa's defensive function by means of increasing the proliferation of intestinal epithelial cells.

关键词： Dachengqi Tang granule intestinal epithelial cell defensive function proliferation

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