Tissue Barriers最新文献

{"title":"Caught red feathered: infection from cockatoo to human and mice reveals genetic plasticity of <i>Cryptococcus neoformans</i> during mammalian passage.","authors":"Dorrian G Cohen, Rebecca A Wingert","doi":"10.1080/21688370.2024.2309717","DOIUrl":"https://doi.org/10.1080/21688370.2024.2309717","url":null,"abstract":"<p><p>The fungus <i>Cryptococcus neoformans</i> is pervasive in our environment and causes the infectious disease cryptococcosis in humans, most commonly in immunocompromised patients. In addition to corroborating the avian origins of a case of cryptococcosis in an immunocompromised patient in 2000, a fascinating recent report has now characterized the genetic and phenotypic changes that occur in this <i>C. neoformans</i> during passage in mammalian hosts. Interestingly, mouse-passaged isolates showed differences in virulence factors ranging from capsule size, melanization, nonlytic macrophage exocytosis, and amoeba predation resistance as compared to the patient strain. Taken together, these results provide new insights about the relationship between mutations acquired during an infection and changes in virulence.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2309717"},"PeriodicalIF":3.1,"publicationDate":"2024-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139571371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive overview of advanced dynamic <i>in vitro</i> intestinal and hepatic cell culture models.","authors":"Filipa Leal, Scarlett Zeiringer, Ramona Jeitler, Pedro F Costa, Eva Roblegg","doi":"10.1080/21688370.2022.2163820","DOIUrl":"10.1080/21688370.2022.2163820","url":null,"abstract":"<p><p>Orally administered drugs pass through the gastrointestinal tract before being absorbed in the small intestine and metabolised in the liver. To test the efficacy and toxicity of drugs, animal models are often employed; however, they are not suitable for investigating drug-tissue interactions and making reliable predictions, since the human organism differs drastically from animals in terms of absorption, distribution, metabolism and excretion of substances. Likewise, simple static <i>in vitro</i> cell culture systems currently used in preclinical drug screening often do not resemble the native characteristics of biological barriers. Dynamic models, on the other hand, provide <i>in vivo</i>-like cell phenotypes and functionalities that offer great potential for safety and efficacy prediction. Herein, current microfluidic <i>in vitro</i> intestinal and hepatic models are reviewed, namely single- and multi-tissue micro-bioreactors, which are associated with different methods of cell cultivation, <i>i.e</i>., scaffold-based <i>versus</i> scaffold-free.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2163820"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9103818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"House dust mite and Th2 cytokine-mediated epithelial barrier dysfunction attenuation by KL001 in 16-HBE cells.","authors":"Santhosh Kumar Duraisamy, Ashokkumar Srinivasan, Isaac Kirubakaran Sundar","doi":"10.1080/21688370.2023.2203841","DOIUrl":"10.1080/21688370.2023.2203841","url":null,"abstract":"<p><p>House dust mite (HDM) is a common aeroallergen that can disrupt the airway epithelial barrier leading to dysregulated immune response, resulting in allergic lung diseases such as asthma. Cryptochrome (CRY), a circadian clock gene, plays an important role in the regulation of metabolism, and immune response. It remains unclear whether stabilizing CRY using KL001 can attenuate HDM/Th2 cytokine-induced epithelial barrier dysfunction in 16-HBE cells. We evaluate the effect of KL001 (20 µM) pre-treatment (4 hrs) in HDM/Th2 cytokine (IL-4 or IL-13)-mediated change in epithelial barrier function. HDM and Th2 cytokine-induced changes in transepithelial electrical resistance (TEER) were determined by an xCELLigence real-time cell analyzer and delocalization of adherens junction complex (AJC: E-cadherin and β-catenin) and tight junction proteins (TJP: Occludin and Zonula occludens-1) by immunostaining and confocal microscopy. Finally, quantitative real-time PCR (qRT-PCR) and Western blotting were used to measure altered gene expression and protein abundance of the epithelial barrier function and core clock genes, respectively. HDM and Th2 cytokine treatment significantly decreased TEER associated with altered gene expression and protein abundance of the selected epithelial barrier function and circadian clock genes. However, pre-treatment with KL001 attenuated HDM and Th2 cytokine-induced epithelial barrier dysfunction as early as 12-24 hrs. KL001 pre-treatment showed attenuation of HDM and Th2 cytokine-induced alteration in the localization and gene expression of AJP and TJP (<i>Cdh1, Ocln,</i> and <i>Zo1</i>) and core clock genes (<i>Clock, Arntl/Bmal1, Cry1/2, Per1/2, Nr1d1/Rev-erbα,</i> and <i>Nfil3</i>). We demonstrate, for the first time, the protective role of KL001 in HDM and Th2 cytokine-mediated epithelial barrier dysfunction.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2203841"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9753958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yogurt starter strains ameliorate intestinal barrier dysfunction via activating AMPK in Caco-2 cells.","authors":"Kyosuke Kobayashi, Junko Mochizuki, Fuka Yamazaki, Toshihiro Sashihara","doi":"10.1080/21688370.2023.2184157","DOIUrl":"10.1080/21688370.2023.2184157","url":null,"abstract":"<p><p>Lactic acid bacteria (LAB) are commonly used probiotics that improve human health in various aspects. We previously reported that yogurt starter strains, <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> 2038 and <i>Streptococcus thermophilus</i> 1131, potentially enhance the intestinal epithelial barrier function by inducing the expression of antimicrobial peptides in the small intestine. However, their effects on physical barrier functions remain unknown. In this study, we found that both strains ameliorated the decreased trans-epithelial resistance and the increased permeability of fluorescein isothiocyanate-dextran induced by tumor necrosis factor (TNF)-α and interferon (IFN)-γ in Caco-2 cells. We also demonstrated that LAB prevented a decrease in the expression and disassembly of tight junctions (TJs) induced by TNF-α and IFN-γ. To assess the repair activity of TJs, a calcium switch assay was performed. Both strains were found to promote the reassembly of TJs, and their activity was canceled by the inhibitor of AMP-activated protein kinase (AMPK). Moreover, these strains showed increased AMPK phosphorylation. These observations suggest that the strains ameliorated physical barrier dysfunction via the activation of AMPK. The activities preventing barrier destruction induced by TNF-α and IFN-γ were strain-dependent. Several strains containing <i>L. bulgaricus</i> 2038 and <i>S. thermophilus</i> 1131 significantly suppressed the barrier impairment, and <i>L. bulgaricus</i> 2038 showed the strongest activity among them. Our findings suggest that the intake of <i>L. bulgaricus</i> 2038 and <i>S. thermophilus</i> 1131 is a potential strategy for the prevention and repair of leaky gut.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2184157"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10859859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Matrix metalloproteinase-7 and claudin-7 as novel identified therapeutic targets for restoration of intestinal epithelial barrier in inflammatory bowel diseases.","authors":"Sunisa Hankan, Pawin Pongkorpsakol","doi":"10.1080/21688370.2023.2182117","DOIUrl":"10.1080/21688370.2023.2182117","url":null,"abstract":"<p><p>Intestinal tight junction disruption and mucosal immune dysregulation contribute to pathogenesis and progression of inflammatory bowel diseases (IBD). A proteolytic enzyme matrix metalloproteinase 7 (MMP-7), which is highly expressed in intestinal tissue, is implicated to IBD and other immune overactivation-associated diseases. In the issue of the Frontiers in Immunology, Ying Xiao and colleagues demonstrate that MMP-7-mediated claudin-7 degradation promotes IBD pathogenesis and disease progression. Therefore, inhibition of MMP-7 enzymatic activity can be a therapeutic strategy for the treatment of IBD.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2182117"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9315537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tight junction and kidney stone disease.","authors":"Papart Rungrasameviriya, Aticha Santilinon, Palita Atichartsintop, Sudarat Hadpech, Visith Thongboonkerd","doi":"10.1080/21688370.2023.2210051","DOIUrl":"10.1080/21688370.2023.2210051","url":null,"abstract":"<p><p>Defects of tight junction (TJ) are involved in many diseases related to epithelial cell functions, including kidney stone disease (KSD), which is a common disease affecting humans for over a thousand years. This review provides brief overviews of KSD and TJ, and summarizes the knowledge on crystal-induced defects of TJ in renal tubular epithelial cells (RTECs) in KSD. Calcium oxalate (CaOx) crystals, particularly COM, disrupt TJ via p38 MAPK and ROS/Akt/p38 MAPK signaling pathways, filamentous actin (F-actin) reorganization and α-tubulin relocalization. Stabilizing p38 MAPK signaling, reactive oxygen species (ROS) production, F-actin and α-tubulin by using SB239063, N-acetyl-L-cysteine (NAC), phalloidin and docetaxel, respectively, successfully prevent the COM-induced TJ disruption and malfunction. Additionally, genetic disorders of renal TJ, including mutations and single nucleotide polymorphisms (SNPs) of CLDN2, CLDN10b, CLDN14, CLDN16 and CLDN19, also affect KSD. Finally, the role of TJ as a potential target for KSD therapeutics and prevention is also discussed.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2210051"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9494007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genital epithelial barrier function is conserved by intravaginal rings releasing etonogestrel and ethinyl estradiol.","authors":"Mohan Liu, Rodolfo D Vicetti Miguel, Nirk E Quispe Calla, Kristen M Aceves, Linda Fritts, Christopher J Miller, John A Moss, Marc M Baum, Thomas L Cherpes","doi":"10.1080/21688370.2023.2186672","DOIUrl":"10.1080/21688370.2023.2186672","url":null,"abstract":"<p><p>The injectable progestin depot-medroxyprogesterone acetate (DMPA) is a popular contraceptive choice in sub-Saharan Africa although mouse models indicate it weakens genital epithelial integrity and barrier function and increases susceptibility to genital infection. The intravaginal ring NuvaRing® is another contraceptive option that like DMPA suppresses hypothalamic pituitary ovarian (HPO) axis function with local release of progestin (etonogestrel) and estrogen (ethinyl estradiol). As we previously reported that treating mice with DMPA and estrogen averts the loss of genital epithelial integrity and barrier function induced by DMPA alone, in the current investigation we compared genital levels of the cell-cell adhesion molecule desmoglein-1 (DSG1) and genital epithelial permeability in rhesus macaques (RM) treated with DMPA or a NuvaRing®re-sized for RM (N-IVR). While these studies demonstrated comparable inhibition of the HPO axis with DMPA or N-IVR, DMPA induced significantly lower genital DSG1 levels and greater tissue permeability to intravaginally administered low molecular mass molecules. By identifying greater compromise of genital epithelial integrity and barrier function in RM administered DMPA vs. N-IVR, our results add to the growing body of evidence that indicate DMPA weakens a fundamental mechanism of anti-pathogen host defense in the female genital tract.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2186672"},"PeriodicalIF":3.1,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10832912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9092932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Submandibular gland epithelial development and the importance of junctions.","authors":"Hélène Bonnet, Carlos Agustin Isidro Alonso, Indra R Gupta","doi":"10.1080/21688370.2022.2161255","DOIUrl":"10.1080/21688370.2022.2161255","url":null,"abstract":"<p><p>Salivary glands consist of highly specialized epithelial cells that secrete the fluid, saliva, and/or transport saliva into the oral cavity. Saliva is essential to lubricate the oral cavity for food consumption and to maintain the hygiene of the oral cavity. In this review, we will focus on the formation of the epithelial cell lineage and the cell junctions that are essential for formation of saliva and maintenance of the epithelial barrier between the ducts that transport saliva and the extracellular environment.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2161255"},"PeriodicalIF":3.1,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10606785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10501270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trans-Compartmental Regulation of Tight Junction Barrier Function.","authors":"Amna N Naser,&nbsp;Qun Lu,&nbsp;Yan-Hua Chen","doi":"10.1080/21688370.2022.2133880","DOIUrl":"10.1080/21688370.2022.2133880","url":null,"abstract":"<p><p>Tight junctions (TJs) are the most apical components of junctional complexes in epithelial and endothelial cells. Barrier function is one of the major functions of TJ, which restricts the ions and small water-soluble molecules from passing through the paracellular pathway. Adherens junctions (AJs) play an important role in cell-cell adhesion and cell signaling. Gap junctions (GJs) are intercellular channels regulating electrical and metabolic signals between cells. It is well known that TJ integral membrane proteins, such as claudins and occludins, are the molecular building blocks responsible for TJ barrier function. However, recent studies demonstrate that proteins of other junctional complexes can influence and regulate TJ barrier function. Therefore, the crosstalk between different cell junctions represents a common means to modulate cellular activities. In this review, we will discuss the interactions among TJ, AJ, and GJ by focusing on how AJ and GJ proteins regulate TJ barrier function in different biological systems.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2133880"},"PeriodicalIF":3.1,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b4/b5/KTIB_11_2133880.PMC10606786.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9769828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antenatal Ureaplasma infection induces ovine small intestinal goblet cell defects: a strong link with NEC pathology.","authors":"Charlotte van Gorp,&nbsp;Ilse H de Lange,&nbsp;Matthias C Hütten,&nbsp;Carmen López-Iglesias,&nbsp;Kimberly Ri Massy,&nbsp;Lilian Kessels,&nbsp;Boris Kramer,&nbsp;Willine van de Wetering,&nbsp;Brad Spiller,&nbsp;George M Birchenough,&nbsp;Wim G van Gemert,&nbsp;Luc J Zimmermann,&nbsp;Tim Gam Wolfs","doi":"10.1080/21688370.2022.2158016","DOIUrl":"10.1080/21688370.2022.2158016","url":null,"abstract":"<p><p>Disruption of the intestinal mucus barrier and intestinal epithelial endoplasmic reticulum (ER) stress contribute to necrotizing enterocolitis (NEC). Previously, we observed intestinal goblet cell loss and increased intestinal epithelial ER stress following chorioamnionitis. Here, we investigated how chorioamnionitis affects goblet cells by assessing their cellular characteristics. Importantly, goblet cell features are compared with those in clinical NEC biopsies. Mucus thickness was assessed as read-out of goblet cell function. Fetal lambs were intra-amniotically (IA) infected for 7d at 122 gestational age with <i>Ureaplasma parvum serovar-3</i>, the main microorganism clinically associated with chorioamnionitis. After preterm delivery, mucus thickness, goblet cell numbers, gut inflammation, epithelial proliferation and apoptosis and intestinal epithelial ER stress were investigated in the terminal ileum. Next, goblet cell morphological alterations (TEM) were studied and compared to human NEC samples. Ileal mucus thickness and goblet cell numbers were elevated following IA UP exposure. Increased pro-apoptotic ER stress, detected by elevated CHOP-positive cell counts and disrupted organelle morphology of secretory cells in the intestinal epithelium, was observed in IA UP exposed animals. Importantly, comparable cellular morphological alterations were observed in the ileum from NEC patients. In conclusion, UP-driven chorioamnionitis leads to a thickened ileal mucus layer and mucus hypersecretion from goblet cells. Since this was associated with pro-apoptotic ER stress and organelle disruption, mucus barrier alterations seem to occur at the expense of goblet cell resilience and may therefore predispose to detrimental intestinal outcomes. The remarkable overlap of these <i>in utero</i> findings with observations in NEC patients underscores their clinical relevance.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2158016"},"PeriodicalIF":3.1,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d9/87/KTIB_11_2158016.PMC10606782.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10476492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}