Tissue Barriers最新文献_第2页

An agonist of the cannabinoid-sensing G-protein coupled receptor 55 promotes wound healing and protects against UVB-induced keratinocyte damage. 大麻素感应g蛋白偶联受体55的激动剂促进伤口愈合并保护免受uvb诱导的角质细胞损伤。

IF 3.1

Tissue Barriers Pub Date : 2026-08-05 DOI: 10.1080/21688370.2026.2713791

Pimngeon Chatkul, Apiwan Arinno, Lapasrada Panpoca, Mathusorn Wongsawat, Pichayapa Sukmak, Phachara Lamlertthon, Nannaphat Suwannakul, Nichakorn Thampathomwong, Pitsinee Supapol, Wanapas Wachiradejkul, Tadhi Sucharitakul, Dollapak Sakulpanich, Switta Kiattikhunphan, Wilasinee Satianrapapong, Thivaratana Sinthuwiwat, Wares Chancharoen, Thiansin Liamsuwan, Pawin Pongkorpsakol

{"title":"An agonist of the cannabinoid-sensing G-protein coupled receptor 55 promotes wound healing and protects against UVB-induced keratinocyte damage.","authors":"Pimngeon Chatkul, Apiwan Arinno, Lapasrada Panpoca, Mathusorn Wongsawat, Pichayapa Sukmak, Phachara Lamlertthon, Nannaphat Suwannakul, Nichakorn Thampathomwong, Pitsinee Supapol, Wanapas Wachiradejkul, Tadhi Sucharitakul, Dollapak Sakulpanich, Switta Kiattikhunphan, Wilasinee Satianrapapong, Thivaratana Sinthuwiwat, Wares Chancharoen, Thiansin Liamsuwan, Pawin Pongkorpsakol","doi":"10.1080/21688370.2026.2713791","DOIUrl":"https://doi.org/10.1080/21688370.2026.2713791","url":null,"abstract":"The use of cannabinoid has been implicated in the treatment of various skin disorders with obscure mechanism of action. This study aimed to investigate the physiological roles of GPR55 in regenerating skin wounds and protecting keratinocyte apoptosis induced by UVB radiation. Here, we found that O1602, a GPR55 agonist, accelerated wound healing in keratinocyte-like HaCaT cells, and this effect was suppressed by pretreatment with inhibitors of protein kinase A (PKA), AMP-activated protein kinase (AMPK), sirtuin-1 (SIRT-1), and extracellular signal-regulated kinase (ERK). Although O1602 treatment promoted keratinocyte proliferation in HaCaT cell line but its proliferative effect did not contribute to enhancing wound healing. Indeed, O1602 upregulated expression of MMP-9, suggesting the stimulation of cell migration. O1602 treatment protected against UVB-induced keratinocyte apoptosis, and this effect was abolished by pretreatment with inhibitors belonging to the same class as that which suppressed the wound-healing response. Furthermore, western blotting analyses revealed that O1602 treatment induced AMPK phosphorylation, and this effect was inhibited by pretreatment of PKA inhibitor. Moreover, O1602 promoted ERK phosphorylation, and this effect was aborted by pretreatment of either AMPK inhibitor or SIRT-1 inhibitor. Enzymatic activation of SIRT-1 induced by O1602 was absent in AMPK inhibitor-pretreated HaCaT cells. Altogether, GPR55 mediates keratinocyte regeneration and exhibits its protective effect against UVB exposure via PKA/AMPK/SIRT-1/ERK-dependent mechanism.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2713791"},"PeriodicalIF":3.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148680286","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}

引用次数: 0

Irisin-treated microbiota restore blood-testis barrier integrity and spermatogenesis in chronically stressed rats. 鸢尾素处理的微生物群恢复慢性应激大鼠血睾丸屏障完整性和精子发生。

IF 3.1

Tissue Barriers Pub Date : 2026-07-24 DOI: 10.1080/21688370.2026.2700679

Itishree Dubey, Manisha Yadav, Sapana Kushwaha

{"title":"Irisin-treated microbiota restore blood-testis barrier integrity and spermatogenesis in chronically stressed rats.","authors":"Itishree Dubey, Manisha Yadav, Sapana Kushwaha","doi":"10.1080/21688370.2026.2700679","DOIUrl":"https://doi.org/10.1080/21688370.2026.2700679","url":null,"abstract":"Chronic psychological stress impairs male fertility by disrupting spermatogenesis and the blood-testis barrier (BTB), which is essential for testicular function. Irisin, a myokine/adipokine involved in metabolic regulation, protects against testicular dysfunction and may beneficially modulate gut microbiota, highlighting its potential in the gut-testis axis. This study investigated the effect of fecal microbiota transplantation (FMT) from irisin-treated rats in restoring BTB integrity in a chronic unpredictable stress (CUS) rat model. Male Sprague-Dawley rats were randomized into four groups: Control, CUS, CUS + Control-FMT, and CUS + Irisin-FMT. CUS-exposed rats received FMT (5 mL, intra-rectally, on alternate days for 2 weeks) from donors treated with either irisin (100 ng/kg, subcutaneously, 4 weeks) or vehicle. The CUS + Irisin-FMT group showed marked improvements in sperm quality, and hormonal profiles, including testosterone, LH, FSH, and irisin. Irisin-FMT increased crypt length, goblet cells, and histological scores, and improved the testicular histological structure and Johnsen's index. These effects were accompanied by upregulation of BTB proteins, E- and N-cadherin, spermatogonia markers, suppression of inflammatory markers (NF-κB, IL-1β, IL-6), and activation of integrin-FAK/Akt/mTOR signaling. Microbiota analysis revealed an increase in beneficial genera, including Lactobacillus and Blautia, as well as the restoration of key families and phyla. Dysbiosis promotes systemic inflammation by altering butyrate and acetate, impairing BTB integrity and testicular function via immune activation, oxidative stress, and endocrine disruption. Irisin-FMT mitigates stress-induced testicular dysfunction by modulating gut microbiota and activating protective signaling pathways, highlighting a novel microbiome-based strategy for male infertility.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2700679"},"PeriodicalIF":3.1,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148585194","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}

引用次数: 0

Modeling tonsil organoids for studying mucosal immune responses to SARS-CoV-2 vaccination. 模拟扁桃体类器官以研究粘膜对SARS-CoV-2疫苗的免疫反应。

IF 3.1

Tissue Barriers Pub Date : 2026-07-19 DOI: 10.1080/21688370.2026.2700690

Yang Gao, Wan Wang, Ying-Ying Wang, Bao-Feng Wang, Jing-Ying Ye

{"title":"Modeling tonsil organoids for studying mucosal immune responses to SARS-CoV-2 vaccination.","authors":"Yang Gao, Wan Wang, Ying-Ying Wang, Bao-Feng Wang, Jing-Ying Ye","doi":"10.1080/21688370.2026.2700690","DOIUrl":"https://doi.org/10.1080/21688370.2026.2700690","url":null,"abstract":"A key bottleneck in preclinical vaccine research is the lack of a human in vitro system that faithfully models the germinal center (GC) reactions, a critical process for generating protective antibodies. This gap hinders the accurate assessment of vaccine candidates. The tonsil is a key component of the mucosal immune system in the oropharynx, acting as its first-line immune sentinel. We established a novel human tonsil organoid platform and stimulated it with the chimpanzee adenovirus serotype 68-19 spike protein (AdC68-19S) SARS-CoV-2 vaccine candidate. Cellular immune phenotypes were analyzed by flow cytometry, while spatial organization was assessed via immunofluorescence. Functional immune responses were quantified using enzyme-linked immunosorbent assay, enzyme-linked immunospot assay, and pseudovirus neutralization tests to measure antigen-specific antibodies production and their neutralizing capacity. AdC68‑19S immunization elicited coordinated GC reactions in tonsil organoids, characterized spatially by the formation of discrete GC compartments, specifically an AICDA+ dark zone and a PD‑1+ light zone. This reorganization was accompanied by a marked expansion of key effector populations, including GC B cells and plasma cells. Functionally, the platform generated antibody‑secreting cells as well as antigen‑specific IgG and IgA antibodies, these antibodies demonstrated neutralizing capacity against the SARS‑CoV‑2 pseudovirus. The human tonsil organoids platform represents a paradigm shift in vitro immunology, establishing a system that recapitulates key features of adaptive immune responses induced by AdC68-19S vaccine. This approach provides a robust, physiologically relevant, and ethically viable model to advance our understanding of human immunity, oral immune barrier and accelerate vaccine development.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2700690"},"PeriodicalIF":3.1,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521088","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}

引用次数: 0

Claudins as signaling hubs of fibrosis, autophagy, and metabolism. Claudins作为纤维化、自噬和代谢的信号中枢。

IF 3.1

Tissue Barriers Pub Date : 2026-07-16 DOI: 10.1080/21688370.2026.2703918

Haruna Fukunaga, Yuki Niwa, Masuo Kondoh

引用次数: 0

Intestine organotypic culture recapitulates human embryonic villus morphogenesis at week 8. 肠器官型培养在第8周重现了人胚胎绒毛的形态发生。

IF 3.1

Tissue Barriers Pub Date : 2026-07-15 DOI: 10.1080/21688370.2026.2700689

Melis Asal, Nanne J Paauw, Maria Thon, Taco Waaijman, Andrew I Morrison, Puck P Mulder, Bernadette S de Bakker, Hetty J Bontkes, Sandra J van Vliet, Reina E Mebius, Susan Gibbs

{"title":"Intestine organotypic culture recapitulates human embryonic villus morphogenesis at week 8.","authors":"Melis Asal, Nanne J Paauw, Maria Thon, Taco Waaijman, Andrew I Morrison, Puck P Mulder, Bernadette S de Bakker, Hetty J Bontkes, Sandra J van Vliet, Reina E Mebius, Susan Gibbs","doi":"10.1080/21688370.2026.2700689","DOIUrl":"https://doi.org/10.1080/21688370.2026.2700689","url":null,"abstract":"The human small intestine depends on villi to generate the large absorptive surface area required for nutrient uptake and barrier integrity. Existing human in vitro models fail to reproduce early villus morphogenesis, as they lack developmental signaling and epithelial-mesenchymal interactions that drive villus initiation. Such models are crucial for understanding the mechanisms of human villus formation to study intestinal development and disease. This study aimed to establish a human organotypic intestine model that recapitulates early villus development and to compare its features with human embryos. Primary organoid-derived epithelial cells containing intestinal stem and progenitor populations, and Caco-2/HT29 cocultures (as reference) were both cultured on a hydrogel containing primary small-intestinal stromal cells in a Transwell system. Models were assessed by histology, electron microscopy, transepithelial electrical resistance (TEER), permeability assays, gene expression analysis, growth factor secretion, and comparison with human embryonic duodenum (Carnegie stages 20-23). Both models formed polarized epithelial monolayers with sparse microvilli compared with mature in vivo intestine. Strikingly, only the organoid-derived model generated stromal cell and extracellular matrix (ECM)-filled epithelial protrusions with localized laminin deposition. This model activated key developmental pathways (SHH, PDGF-AA, BMP4, and WNT5A), upregulated villus-associated transcription factors (FOXF1, FOXF2, and FOXL1), and expressed laminin isoforms linked to villus initiation. The morphology and height of the protrusions (approx. 28 µm) closely resembled early villi in Carnegie stage 21 embryos.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2700689"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148456932","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}

引用次数: 0

Erlotinib impairs epidermal tight junction and barrier integrity by inhibiting EGFR and Src and affects maturation of cell-cell junctions in human and mouse keratinocytes. 厄洛替尼通过抑制EGFR和Src损害表皮紧密连接和屏障完整性，并影响人和小鼠角质形成细胞中细胞-细胞连接的成熟。

IF 3.1

Tissue Barriers Pub Date : 2026-07-13 DOI: 10.1080/21688370.2026.2696758

Keisuke Imafuku, Alexander Garcia-Ponce, Jens Waschke

{"title":"Erlotinib impairs epidermal tight junction and barrier integrity by inhibiting EGFR and Src and affects maturation of cell-cell junctions in human and mouse keratinocytes.","authors":"Keisuke Imafuku, Alexander Garcia-Ponce, Jens Waschke","doi":"10.1080/21688370.2026.2696758","DOIUrl":"https://doi.org/10.1080/21688370.2026.2696758","url":null,"abstract":"Erlotinib, an epidermal growth factor receptor (EGFR) inhibitor, is widely used in cancer therapy but frequently causes cutaneous adverse effects that suggest impairment of the epidermal barrier. To better understand the underlying mechanisms, we examined how erlotinib affects barrier integrity, with a focus on tight junctions (TJs) and their relation with the actin cytoskeleton. Using human and mouse ex vivo epidermis as well as cultured keratinocytes, we assessed junctional assembly and stability under pharmacological inhibition of EGFR and Src. Erlotinib treatment disrupted the epithelial barrier, as demonstrated by enhanced biotin tracer penetration and a marked reduction in transepithelial electrical resistance. In line with functional impairment, erlotinib reduced EGFR and Src activity disturbing maturation of junctions, as evidenced by discontinuous claudin-1 and ZO-1 localization. Furthermore, erlotinib induced a loss of the apically localized tension-sensitive conformation of α-catenin in the stratum granulosum and in cultured keratinocytes. This was accompanied by disorganization of cortical actin and increased presence of stress fibers, in parallel with elevated activation of RhoA and phosphorylation of MLC2. Inhibition of Src with PP2 led to similar effects on barrier integrity. However, this detrimental outcome could be rescued by EGF treatment. Together, these findings indicate that erlotinib impairs epidermal barrier function by affecting junctional maturation via disrupted α-catenin membrane distribution, and ultimately, TJ stability involving intracellular contraction and tension. Thus, strategies focused on targeting tension‑related mechanisms downstream of EGFR/Src might help prevent or alleviate the cutaneous toxicities associated with EGFR inhibitory therapies.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2696758"},"PeriodicalIF":3.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148438095","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}

引用次数: 0

A Dsg3-specific pemphigus autoantibody induces formation of immature desmosomes associated with impaired adhesion. dsg3特异性天疱疮自身抗体诱导与粘附受损相关的未成熟桥粒的形成。

IF 3.1

Tissue Barriers Pub Date : 2026-07-10 DOI: 10.1080/21688370.2026.2700483

Julia Huber, Michael Fuchs, Jens Waschke, Christoph Hudemann, Lukas F Reissig, Thomas Schmitt

{"title":"A Dsg3-specific pemphigus autoantibody induces formation of immature desmosomes associated with impaired adhesion.","authors":"Julia Huber, Michael Fuchs, Jens Waschke, Christoph Hudemann, Lukas F Reissig, Thomas Schmitt","doi":"10.1080/21688370.2026.2700483","DOIUrl":"https://doi.org/10.1080/21688370.2026.2700483","url":null,"abstract":"Pemphigus is a severe blistering autoimmune disease in which autoantibodies against the desmosomal cadherins Dsg1 and Dsg3 cause loss of desmosome adhesion. It is hypothesized that this loss of adhesion results from a combination of direct inhibition of cadherin interaction and subsequent downstream signaling events impairing desmosome turnover and maturation. In this study, we combined dissociation assays with super-resolution STED microscopy to investigate desmosome ultrastructural features as markers for turnover and maturation. Immunostaining, super-resolution STimulated Emission Depletion (STED) microscopy, SUper resolution SHadow Imaging (SUSHI), Ca2+-depletion-repletion, dispase-based dissociation assay, Western blot analysis. We found that desmosome number, plaque distance, plaque thickness and intercellular widening are reliable parameters correlating with adhesive strength. These parameters, as well as accumulation of Dsg1 at cell borders, also appear to be good delineators for desmosome maturation. E-Cadherin and EGFR incorporation on the other hand occur only at very early stages of desmosome recovery or dependent on other factors and therefore appear to be less reliable indicators. We further show that the Dsg3-specific pemphigus antibody AK23 or AK23 Fab also partially reverted desmosomes to an immature stage. Lastly, we observed that cAMP accelerates whereas Src slows desmosome recovery. This study supports the hypothesis that autoantibodies in pemphigus interfere with desmosome recovery and maturation, which can be reliably investigated using super-resolution microscopy. Considering the current state of the art, detailed investigation of pathways involved in the regulation of desmosome turnover and maturation may provide valuable insights for future treatment strategies.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2700483"},"PeriodicalIF":3.1,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424664","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}

引用次数: 0

Blood-brain barrier permeability in diffuse large B-Cell lymphoma: associations with established risk factors for CNS relapse. 弥漫性大b细胞淋巴瘤的血脑屏障通透性：与中枢神经系统复发的既定危险因素相关

IF 3.1

Tissue Barriers Pub Date : 2026-07-04 DOI: 10.1080/21688370.2026.2696764

Martine Prütz Nørskov, Elisabeth Præstekjær Cramer, Ulrich Lindberg, Adam Espe Hansen, Jonathan Frederik Carlsen, Peter de Nully Brown, Henrik Bo Wiberg Larsson, Martin Hutchings, Stig Præstekjær Cramer

{"title":"Blood-brain barrier permeability in diffuse large B-Cell lymphoma: associations with established risk factors for CNS relapse.","authors":"Martine Prütz Nørskov, Elisabeth Præstekjær Cramer, Ulrich Lindberg, Adam Espe Hansen, Jonathan Frederik Carlsen, Peter de Nully Brown, Henrik Bo Wiberg Larsson, Martin Hutchings, Stig Præstekjær Cramer","doi":"10.1080/21688370.2026.2696764","DOIUrl":"https://doi.org/10.1080/21688370.2026.2696764","url":null,"abstract":"Central nervous system (CNS) relapse is a serious complication of diffuse large B-Cell lymphoma (DLBCL), often associated with poor clinical outcomes. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) enables detection of subtle blood-brain barrier (BBB) leakage. We assessed BBB permeability, using the Patlak model, in 63 patients with DLBCL without CNS involvement and 11 healthy controls using DCE-MRI, and investigated associations with established risk factors for CNS relapse. Patients with high risk of CNS relapse (CNS-IPI ≥4) demonstrated near-significant increased BBB permeability in cortical gray matter (GM) compared with both low-risk patients (p = 0.053) and healthy controls (p = 0.02). BBB permeability in cortical GM and in cerebral white matter (WM) correlated positively with age (p < 0.001). After adjusting for age, patients with kidney and/or adrenal involvement exhibited significantly higher BBB permeability in cortical GM (p = 0.04). Furthermore, plasma albumin levels were inversely correlated with BBB permeability in both GM (p = 0.003) and WM (p = 0.005). These findings indicate that subclinical BBB dysfunction may contribute to CNS vulnerability in DLBCL, potentially predisposing patients to relapse even before CNS involvement occurs. The observed age-related increase in BBB permeability is consistent with previous reports and may represent an independent risk for CNS relapse. Collectively, these results suggest that BBB imaging could improve CNS risk stratification in DLBCL. Prospective studies are warranted to determine whether early BBB alterations can predict CNS relapse in individual patients.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2696764"},"PeriodicalIF":3.1,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148388254","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}

引用次数: 0

Developmental maturation of intestinal junctional complexes in preterm infants. 早产儿肠结复合体的发育成熟。

IF 3.1

Tissue Barriers Pub Date : 2026-07-02 DOI: 10.1080/21688370.2026.2697088

Catherine Kollmann, Carolin Niklas, Karen Ernestus, Grit Gesine Ruth Hiller, Marius Hörner, Natalie Burkard, Christoph-Thomas Germer, Christoph Härtel, Sina Bartfeld, Kirsten Glaser, Nicolas Schlegel

{"title":"Developmental maturation of intestinal junctional complexes in preterm infants.","authors":"Catherine Kollmann, Carolin Niklas, Karen Ernestus, Grit Gesine Ruth Hiller, Marius Hörner, Natalie Burkard, Christoph-Thomas Germer, Christoph Härtel, Sina Bartfeld, Kirsten Glaser, Nicolas Schlegel","doi":"10.1080/21688370.2026.2697088","DOIUrl":"https://doi.org/10.1080/21688370.2026.2697088","url":null,"abstract":"Preterm infants are prone to gastrointestinal complications such as infectious diseases and necrotizing enterocolitis, which are associated with intestinal inflammation and increased intestinal permeability. Intestinal epithelial barrier (IEB) function is known to be immature in preterm neonates; however, our understanding of how the IEB develops - particularly the formation of junctional complexes - remains limited. Here, we analyzed intestinal tissue specimens from healthy resection margins of six very immature preterm infants who underwent bowel resection due to focal intestinal perforation (at the chronological age of 25 to 28 weeks' gestation), and compared the composition of tight junctions, adherens junctions and desmosomes to that of adults. Using immunostaining, our observations show, that tight junction proteins Claudin-2, Claudin-3 and Occludin, adherens junction proteins E-cadherin and β-Catenin as well as desmosomal proteins Plakoglobin and Plakophilin-2 appeared as mature as in adults as early as 25 weeks' gestation. However, Claudin-1, -4 and -5, as well as ZO-1 staining patterns increased and became more defined with increasing gestational age, suggesting junctional maturation during gestational week 26 and 27. Desmosomal protein Desmocollin-2 was increased until 26 weeks' gestation whereas Desmoglein-2 and Desmoplakin expression was immature at 28 weeks' gestation compared to the expression in adults. Our study provides the first sequential characterization of junctional protein maturation across all major IEB components early in life in human samples. These findings may help identify key mechanisms underlying intestinal barrier-associated pathologies in preterm infants.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2697088"},"PeriodicalIF":3.1,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148377198","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}

引用次数: 0

Inflammation and epidermal barrier integrity, decline, and restoration: It's time to rouse the "guardians at the gate". 炎症和表皮屏障的完整性、衰退和恢复：是时候唤醒“门口的守护者”了。

IF 3.1

Tissue Barriers Pub Date : 2026-06-30 DOI: 10.1080/21688370.2026.2696086

Michael L Samulevich, Liam E Carman, Brian J Aneskievich

{"title":"Inflammation and epidermal barrier integrity, decline, and restoration: It's time to rouse the \"guardians at the gate\".","authors":"Michael L Samulevich, Liam E Carman, Brian J Aneskievich","doi":"10.1080/21688370.2026.2696086","DOIUrl":"https://doi.org/10.1080/21688370.2026.2696086","url":null,"abstract":"Epidermal barrier (EB) function is too often reduced to the role of a passive, inanimate upper strata of dead corneocytes surrounded by extruded lipids. However, this summary fails to appreciate the lower strata keratinocytes (KCs) which serve as both sensors and effectors of immune signaling and thus contribute a dynamic, responsive nature to EB and maintenance and possible decline. In this context, underpinnings of chronic inflammatory skin diseases, e.g. psoriasis and atopic dermatitis, can be better recognized as a feed forward loop in which barrier dysfunction and runaway inflammatory signaling reinforce one another. Traditional therapies addressing these diseases focus on quelling effects and activities of pro-inflammatory extracellular cytokines and their cognate receptors. This paradigm overlooks the promising alternative of augmenting endogenous negative regulators of inflammatory signaling, e.g. the proteins A20 (TNFAIP3) and TNIP1 (ABIN-1) which we propose act as \"guardians\" restricting NF-κB-dependent inflammatory pathways. Here, we explore the rationale and possible means for targeting these regulators to protect or restore EB integrity. Bolstering these intrinsic quenchers of inflammatory signal progression may offer a path to restore tissue homeostasis and repair the EB in chronic inflammatory disease states.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2696086"},"PeriodicalIF":3.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353877","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}

引用次数: 0