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Microbiome and intestinal pathophysiology in post-acute sequelae of COVID-19

Genes & Diseases 2024年第3期11卷 220-231页

作者： Jilei Zhang Yongguo Zhang Yinglin Xia Jun Sun Division of Gastroenterology and Hepatology Department of MedicineUniversity of Ilinois ChicagoIL60612USA Uic Cancer Center Department of Microbiology and ImmunologyUniversity of Ilinois ChicagoChicagoIL60612USA Jesse Brown VA Medical Center ChicagoIL60612USA

Long CoVID,also known for post-acute sequelae of CovID-19,describes the people who have the signs and symptoms that continue or develop after the acute coviD-19 phase.Long CovID patients suffer from an inflammation or host responses towards the virus approx-imately 4 weeks after initial infection with the SARS CoV-2 virus and continue for an unchar-acterized duration.Anyone infected with CovID-19 before could experience long-CcovID conditions,including the patients who were infected with SARS CoV-2 virus confirmed by tests and those who never knew they had an infection early.People with long CoviD may experience health problems from different types and combinations of symptoms over time,such as fa-tigue,dyspnea,cognitive impairments,and gastrointestinal(Gl)symptoms(e.g.,nausea,vom-iting,diarrhea,decreased or loss of appetite,abdominal pain,and dysgeusia).The critical role of the microbiome in these Gl symptoms and long CovID were reported in clinical patients and experimental models.Here,we provide an overall view of the critical role of the Gl tract and microbiome in the development of long COVID,including the clinical Gl symptoms in patients,dysbiosis,viral-microbiome interactions,barrier function,and inflammatory bowel disease patients with long CovID.We highlight the potential mechanisms and possible treatment based on Gl health and microbiome.Finally,we discuss challenges and future direction in the long CoVID clinic and research.

关键词： Gastrointestinal symptoms Gl tract Gut microbiome Inflammatorybowel diseases Intestinal barrier Long CoVID Metabolites tight junctions

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Blood-brain barrier pathology in cerebral small vessel disease

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Neural Regeneration Research 2024年第6期19卷 1233-1240页

作者： Ruxue Jia Gemma Solé-Guardia Amanda J.Kiliaan Department of Medical Imaging Anatomy Radboud University Medical Center Donders Institute for Brain Cognition & Behavior Center for Medical Neuroscience Preclinical Imaging Center PRIME Radboud Alzheimer Center

Cerebral small vessel disease is a neurological disease that affects the brain microvasculature and which is commonly observed among the elderly. Although at first it was considered innocuous, small vessel disease is nowadays regarded as one of the major vascular causes of dementia. Radiological signs of small vessel disease include small subcortical infarcts, white matter magnetic resonance imaging hyperintensities, lacunes, enlarged perivascular spaces, cerebral microbleeds, and brain atrophy; however, great heterogeneity in clinical symptoms is observed in small vessel disease patients. The pathophysiology of these lesions has been linked to multiple processes, such as hypoperfusion, defective cerebrovascular reactivity, and blood-brain barrier dysfunction. Notably, studies on small vessel disease suggest that blood-brain barrier dysfunction is among the earliest mechanisms in small vessel disease and might contribute to the development of the hallmarks of small vessel disease. Therefore, the purpose of this review is to provide a new foundation in the study of small vessel disease pathology. First, we discuss the main structural domains and functions of the blood-brain barrier. Secondly, we review the most recent evidence on blood-brain barrier dysfunction linked to small vessel disease. Finally, we conclude with a discussion on future perspectives and propose potential treatment targets and interventions.

关键词： blood-brain barrier dysfunction cerebral blood flow cerebral hypoperfusion endothelial dysfunction hypertension inflammation magnetic resonance imaging neurovascular unit oxidative stress small vessel disease tight junctions transcytosis

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Intestine Enzyme-responsive Polysaccharide-based Hydrogel to Open Epithelial tight junctions for Oral Delivery of Imatinib against Colon Cancer

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Chinese Journal of Polymer Science 2022年第10期40卷 1154-1164,I0007页

作者： Cong-Yu Wang Min Sun Zhen Fan Jian-Zhong Du Department of Polymeric Materials School of Materials Science and EngineeringTongji UniversityShanghai 201804China Department of Gynaecology and Obstetrics Shanghai Fourth People's HospitalSchool of MedicineTongji UniversityShanghai 200434China

Imatinib has been widely used as a selective kinase inhibitor for treating a variety of cancers,and this molecule is very hydrophobic so it is usually modified with mesylate salt in clinic to increase bioavailability.However,pH-dependent aqueous solubility and relatively high dosage of imatinib mesylate greatly reduce the clinical outcomes.To solve this problem,we developed an intestine enzyme-responsive hydrogel to efficiently encapsulate hydrophobic imatinib with long-term controlled release and enhanced intestinal permeability through oral administration.Methacrylic anhydride-modified carboxymethyl chitosan(MA-CMCS)was synthesized via amidation reaction and then MA-CMCS was crosslinked with photoinitator under UV-irradation to form a three-dimensional hydrophilic polymer network.The intestine enzyme responsiveness was endowed with imatinib-loaded hydrogel through hydrolyzation of glucosidic bond,which could achieve enzyme-triggered long-term drug release of up to 2 days.Furthermore,sodium deoxycholate was embedded into the hydrogel to synchronously open epithelial tight junctions with improved intestinal permeability.In vitro studies revealed similar lethality against colon cancer cell for both imatinib mesylate and imatinib-loaded hydrogels.Moreover,significantly enhanced in vivo tumor inhibition(6-fold higher compared to imatinib mesylate)was achieved after oral administration with imatinib-loaded hydrogels.Overall,this enzyme-responsive hydrogel could achieve long-term synchronous release of kinase inhibitor(imatinib)and tight junction permeation enhancer(sodium deoxycholate)at intestine with enhanced therapeutic efficiency,which could provide an effective approach to improve the bioavailability of hydrophobic anticancer chemodrugs with oral administration.

关键词： Carboxymethyl chitosan Imatinib Hydrogels Oral delivery tight junctions

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Targeting PKM2 signaling cascade with salvianic acid A normalizes tumor blood vessels to facilitate chemotherapeutic drug delivery

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Acta Pharmaceutica Sinica B 2024年第5期14卷 2077-2096页

作者： Cheng Qian Yueke Zhou Teng Zhang Guanglu Dong Mengyao Song Yu Tang Zhonghong Wei Suyun Yu Qiuhong Shen Wenxing Chen Jaesung P.Choi Juming Yan Chongjin Zhong Li Wan Jia Li Aiyun Wang Yin Lu Yang Zhao Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica Nanjing University of Chinese MedicineNanjing 210023China School of Medicine&Holistic Integrative Medicine Nanjing University of Chinese MedicineNanjing 210023China Centre for Inflammation Faculty of ScienceCentenary InstituteSchool of Life SciencesUniversity of Technology SydneySydney NSW 2050Australia Jiangsu Key Laboratory of Immunity and Metabolism Department of Pathogenic Biology and ImmunologyNational Experimental Demonstration Center for Basic Medicine EducationXuzhou Laboratory of Infection and ImmunityXuzhou Medical UniversityXuzhou 221004China Department of General Surgery Jiangsu Province Hospital of Chinese MedicineAffiliated Hospital of Nanjing University of Chinese MedicineNanjing 210029China Macquarie Medical School Faculty of MedicineHuman Health SciencesMacquarie UniversitySydney NSW 2109Australia

Aberrant tumor blood vessels are prone to propel the malignant progression of tumors,and targeting abnormal metabolism of tumor endothelial cells emerges as a promising option to achieve vascular normalization and antagonize tumor progression.Herein,we demonstrated that salvianic acid A(SAA)played a pivotal role in contributing to vascular normalization in the tumor-bearing mice,thereby improving delivery and effectiveness of the chemotherapeutic agent.SAA was capable of inhibiting glycolysis and strengthening endothelial junctions in the human umbilical vein endothelial cells(HUVECs)exposed to hypoxia.Mechanistically,SAA was inclined to directly bind to the glycolytic enzyme PKM2,leading to a dramatic decrease in endothelial glycolysis.More importantly,SAA improved the endothelial integrity via activating theβ-Catenin/Claudin-5 signaling axis in a PKM2-dependent manner.Our findings suggest that SAA may serve as a potent agent for inducing tumor vascular normalization.

关键词： Salvianic acid A Tumor vascular normalization PKM2 β-Catenin Claudin-5 Endothelial glycolysis tight junctions Doxorubicin

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Hepatic tight junctions:From viral entry to cancer metastasis

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World Journal of Gastroenterology 2010年第3期16卷 289-295页

作者： Nikki P Lee John M Luk Department of Surgery Queen Mary Hospital Department of Pharmacology and Department of Surgery National University Health SystemNational University of Singapore

The tight junction (TJ) is a critical cellular component for maintenance of tissue integrity, cellular interactions and cell-cell communications, and physiologically functions as the "great wall" against external agents and the surrounding hostile environment. During the host-pathogen evolution, viruses somehow found the key to unlock the gate for their entry into cells and to exploit and exhaust the host cells. In the liver, an array of TJ molecules is localized along the bile canaliculi forming the blood-biliary barrier, where they play pivotal roles in paracellular permeability, bile secretion, and cell polarity. In pathology, certain hepatic TJ molecules mediate virus entry causing hepatitis infection; deregulation and functional abnormality of the TJ have also been implicated in triggering liver cancer development and metastasis. All these findings shed new insights on the understanding of hepatic TJs in the development of liver disease and provide new clues for potential intervention.

关键词： tight junctions Hepatocytes Blood-biliary barrier Bile canaliculi Hepatitis Liver steatosis Liver neoplasms

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Role of tight junctions and Their Protein Expression in Atopic Dermatitis

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International Journal of Dermatology and Venereology 2021年第1期4卷 40-44页

作者： Kunwar Namrata Bing-Xue Bai Dermatology and Venereology Department Second Affiliated Hospital of Harbin Medical UniversityHarbinHeilongjiang 150001China

Atopic dermatitis(AD)is a chronic inflammatory skin disease with xerosis,itchiness,as well as interconnection with immunoglobulin E(Ig E),mediated foods including airborne allergies.AD is not only related to the diminished stratum corneum barrier but also presents with an unusual expression of tight junctions(TJs)proteins.TJ barrier dysfunction leads to impairment in the stratum corneum(SC)barrier.The significant role of TJs in the epidermal barrier as indicated by Claudin-1(Cldn-1)deficient mice that undergo high transepidermal water loss(TEWL)and skin dehydration.In atopic dermatitis,downregulation of Cldn-1 was observed due to inflammation.Still,a lack of distinct understanding exists in considering tight junction barrier impairment as a cause or outcome in atopic dermatitis.This review summarizes TJs main role in skin barrier function and TJ proteins(TJPs)expression observed in AD patients.

关键词： atopic dermatitis tight junctions claudin

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Influence of puerarin,paeoniflorin,and menthol on structure and barrier function of tight junctions in MDCK and MDCK-MDR1 Cells

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Journal of Traditional Chinese Medical Sciences 2015年第2期2卷 111-119页

作者： Lin Zhang Shouying Du Yang Lu Chang Liu Huichao Wu Bing Yang Jie Bai Pengyue Li School of Chinese Materia Medica Beijing University of Chinese MedicineBeijing 100029China

Objective:In this study,the influence of puerarin,paeoniflorin,and menthol on the structure and barrier function of tight junctions(TJs)in MadineDarby canine kidney epithelial(MDCK)and MDCK-multi-drug resistance 1(MDR1)cells was evaluated to determine the mechanisms by which the drugs cross the bloodebrain barrier(BBB).Method:Cells were treated with puerarin,paeoniflorin,and menthol followed by immunohistochemical staining with occludin,claudin-1,and F-actin.The cells were then observed using laser-scanning confocal microscopy.Average optical density(AOD)of the immunofluorescence images of the proteins were analyzed using ImageJ software while Transepithelial electrical resistance(TEER)was measured using an epithelial voltohmmeter.Results:Confocal microscopy revealed that puerarin-and paeoniflorin-treated tight junction proteins were conspicuous while menthol suppressed their expression.Correspondingly,AOD values of cells treated with puerarin or paeoniflorin,or both showed no difference compared to the control group(P>.05)while the menthol group value was downregulated.In 3 h,TEER of cells not treated with menthol were similar to the control group,while treatment with menthol significantly decreased TEER value(P<.05).In addition,application of menthol decreased TEER in MDCK cells earlier than in MDCK-MDR1 cells.Conclusion:Menthol but not puerarin and paeoniflorin may enhance paracellular transport and improve drug penetration of the BBB by disrupting the structure and,thereby,weakening the barrier function of TJs.

关键词： Puerarin Paeoniflorin Menthol tight junctions Bloodebrain barrier

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Protocadherin gamma C3:a new player in regulating vascular barrier function

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Neural Regeneration Research 2023年第1期18卷 68-73页

作者： Victoria Kaupp Kinga G.Blecharz-Lang Christina Dilling Patrick Meybohm Malgorzata Burek Department of Anesthesiology Intensive CareEmergency and Pain MedicineUniversity of WürzburgUniversity Hospital WürzburgWürzburgGermany Department of Experimental Neurosurgery Charité-UniversitätsmedizinBerlinGermany

Defects in the endothelial cell barrier accompany diverse malfunctions of the central nervous system such as neurodegenerative diseases,stroke,traumatic brain injury,and systemic diseases such as sepsis,viral and bacterial infections,and cancer.Compromised endothelial sealing leads to leaking blood vessels,followed by vasogenic edema.Brain edema as the most common complication caused by stroke and traumatic brain injury is the leading cause of death.Brain microvascular endothelial cells,together with astrocytes,pericytes,microglia,and neurons form a selective barrier,the so-called blood-brain barrier,which regulates the movement of molecules inside and outside of the brain.Mechanisms that regulate blood-brain barrier permeability in health and disease are complex and not fully understood.Several newly discovered molecules that are involved in the regulation of cellular processes in brain microvascular endothelial cells have been described in the literature in recent years.One of these molecules that are highly expressed in brain microvascular endothelial cells is protocadherin gamma C3.In this review,we discuss recent evidence that protocadherin gamma C3 is a newly identified key player involved in the regulation of vascular barrier function.

关键词： blood-brain barrier brain microvascular endothelial cells permeability protein interaction protocadherin gamma C3 protocadherins tight junctions

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Effects of arginine replacement with L-citrulline on the arginine/nitric oxide metabolism in chickens:An animal model without urea cycle

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Journal of Animal Science and Biotechnology 2023年第3期14卷 1182-1200页

作者： Victoria Anthony Uyanga Lijing Sun Yu Liu Meiming Zhang Jingpeng Zhao Xiaojuan Wang Hongchao Jiao Okanlawon M.Onagbesan Hai Lin Department of Animal Science College of Animal Science and Veterinary MedicineShandong Provincial Key Laboratory of Animal Biotechnology and Disease ControlShandong Agricultural UniversityNo.61 Daizong StreetTai’an CityShandong Province 271018China Department of Animal Physiology Federal University of AgricultureOgun StateAbeokuta P.M.B 2240Nigeria

Background This study examined the efficacy of L-citrulline supplementation on the arginine/nitric oxide metabolism,and intestinal functions of broilers during arginine deficiency.A total of 288 day-old Arbor Acre broilers were randomly assigned to either an arginine deficient basal diet(NC diet),NC diet+0.50%L-arginine(PC diet),or NC diet+0.50%L-citrulline(NCL diet).Production performance was recorded,and at 21 days old,chickens were euthanized for tissue collection.Results The dietary treatments did not affect the growth performance of broilers(P>0.05),although NC diet increased the plasma alanine aminotransferase,urate,and several amino acids,except arginine(Ptight junction proteins(Claudin 1 and Occludin),and intestinal mucosal defense(MUC2 and p Ig R).The intestinal morphology revealed that both PC and NCL diets improved(P<0.05)the ileal VH/CD ratio and the jejunal VH and VH/CD ratio compared to the NC fed broilers.Conclusion This study revealed that NCL diet supported arginine metabolism,nitric oxide synthesis,and promoted the intestinal function of broilers.Thus,L-citrulline may serve as a partial arginine replacement in broiler’s diet without detrimental impacts on the performance,

关键词： Amino acids Arginine Broiler chicken Citrulline Intestinal health Nutrient transporters tight junctions

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Tannic acid assisted anti-TNF-αnanobody assembly modulating the epithelial barrier dysregulation of allergic rhinitis

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Nano Research 2023年第7期16卷 9781-9791页

作者： Shuilian Fu Zhiting Cao Baolian Huang Te Yin Chujun Huang Zhiqian Bi Yingying Yao Xiaoyao Chang Hongqin Zhuang Zi-Chun Hua The State Key Laboratory of Pharmaceutical Biotechnology College of Life SciencesNanjing UniversityNanjing 210023China Changzhou High-Tech Research Institute of Nanjing University and Jiangsu TargetPharma Laboratories Inc. Changzhou 213164China School of Biopharmacy China Pharmaceutical UniversityNanjing 211198China

The derailed nasal epithelial barrier is associated with the disorder of tight junctions(TJ)function or expression,leading to more penetration of allergens to the barrier,accompanied by the release of cytokines,which develop allergic rhinitis(AR).Considering the increasing AR disease incidence worldwide,there is still an urgent unmet medical need to develop new therapeutics.Tumor necrosis factor-alpha(TNF-α)inhibitors have been applied in treating autoimmune diseases.However,their roles in AR remain unclear.In this study,anti-TNF-αnanobody(V)was assembled with tannic acid(V/TA)as a functional antibody drug candidate which could inhibit the release of the cytokines in ovalbumin(OVA)-induced AR murine model.Upon receiving V/TA treatment,the infiltration level of inflammatory cells,and the number of mucus-secreting cells and mast cells in the nasal mucosa recovered to a relatively normal level.Preliminary mechanism of action research revealed that the efficacy of V/TA was accompanied by the restricted level of TJ molecules:zonula occluden-1(ZO-1),occludin,claudin-1,and claudin-5.The therapeutic effect of the anti-TNF-αnanobody against AR was enhanced with the tannic acid assisted without any toxicity observed.This study supplied a promising delivery strategy of TNF-αinhibitor for the effective treatment of complicated allergic rhinitis disease,with an advantage in restoring effect on the AR-caused epithelial barrier defects than the commercial drug Infliximab.

关键词： allergic rhinitis tumor necrosis factor-alpha(TNF-α)nanobody nanoparticles epithelial permeability tight junctions

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