scholarly journals A Gut-Brain Axis-on-a-Chip for studying transport across epithelial and endothelial barriers

2021 ◽  
Author(s):  
Min-Hyeok Kim ◽  
Donghyun Kim ◽  
Jong Hwan Sung
Keyword(s):  
Endothelial Barriers

Ultrastructural studies on the interaction of haemophilus influenzae with human endothelial cells in vitro

1990 ◽  
Vol 48 (3) ◽  
pp. 636-637
Author(s):  
D.J.P. Ferguson ◽  
M. Virji ◽  
H. Kayhty ◽  
E.R. Moxon
Keyword(s):  
Endothelial Cells ◽  
Haemophilus Influenzae ◽  
Intercellular Junctions ◽  
Blood Stream ◽  
Ultrastructural Studies ◽  
Endothelial Barriers ◽  
Serotype B ◽  
Meningitis In Children ◽  
Respiratory Epithelial

Haemophilus influenzae is a human pathogen which causes meningitis in children. Systemic H. influenzae infection is largely confined to encapsulated serotype b organisms and is a major cause of meningitis in the U.K. and elsewhere. However, the pathogenesis of the disease is still poorly understood. Studies in the infant rat model, in which intranasal challenge results in bacteraemia, have shown that H. influenzae enters submucosal tissues and disseminates to the blood stream within minutes. The rapidity of these events suggests that H. influenzae penetrates both respiratory epithelial and endothelial barriers with great efficiency. It is not known whether the bacteria penetrate via the intercellular junctions, are translocated within the cells or carried across the cellular barrier in 'trojan horse' fashion within phagocytes. In the present studies, we have challenged cultured human umbilical cord_vein endothelial cells (HUVECs) with both capsulated (b+) and capsule-deficient (b-) isogenic variants of one strain of H. influenzae in order to investigate the interaction between the bacteria and HUVEC and the effect of the capsule.

scholarly journals Treponema pallidum Disrupts VE-Cadherin Intercellular Junctions and Traverses Endothelial Barriers Using a Cholesterol-Dependent Mechanism

2021 ◽  
Vol 12 ◽  
Author(s):  
Karen V. Lithgow ◽  
Emily Tsao ◽  
Ethan Schovanek ◽  
Alloysius Gomez ◽  
Leigh Anne Swayne ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipid Raft ◽  
Vascular Endothelium ◽  
Immunofluorescence Microscopy ◽  
Treponema Pallidum ◽  
Intercellular Junctions ◽  
Endothelial Barriers ◽  
Junctional Protein ◽  
Gain Access ◽  
Dependent Mechanism

Treponema pallidum subspecies pallidum, the causative agent of syphilis, traverses the vascular endothelium to gain access to underlying tissue sites. Herein, we investigate the mechanisms associated with T. pallidum traversal of endothelial barriers. Immunofluorescence microscopy reveals that a subpopulation of T. pallidum localizes to intercellular junctions and that viable T. pallidum, as well as a T. pallidum vascular adhesin (Tp0751), disrupts the architecture of the main endothelial junctional protein VE-cadherin. Intriguingly, in this study we show that T. pallidum traverses endothelial barriers with no disruption in barrier permeability. Furthermore, barrier traversal by T. pallidum is reduced by pretreatment of endothelial cells with filipin, an inhibitor that blocks cholesterol-mediated endocytosis. Collectively, these results suggest that T. pallidum can use a cholesterol-dependent, lipid raft-mediated endocytosis mechanism to traverse endothelial barriers. Further, treponemal localization to, and disruption of, intercellular junctions suggests that a paracellular route may also be utilized, a dual traversal strategy that has also been observed to occur for leukocytes and other invasive bacteria.

scholarly journals Vav3-induced cytoskeletal dynamics contribute to heterotypic properties of endothelial barriers

2018 ◽  
Vol 217 (8) ◽  
pp. 2813-2830 ◽  
Author(s):  
Georg Hilfenhaus ◽  
Dai Phuong Nguyen ◽  
Jonathan Freshman ◽  
Divya Prajapati ◽  
Feiyang Ma ◽  
...  
Keyword(s):  
Ectopic Expression ◽  
Large Artery ◽  
Nucleotide Exchange ◽  
Nucleotide Exchange Factor ◽  
Cytoskeletal Dynamics ◽  
Endothelial Barriers ◽  
Multiple Cell ◽  
Barrier Resistance ◽  
Cell Matrix Interactions

Through multiple cell–cell and cell–matrix interactions, epithelial and endothelial sheets form tight barriers. Modulators of the cytoskeleton contribute to barrier stability and act as rheostats of vascular permeability. In this study, we sought to identify cytoskeletal regulators that underlie barrier diversity across vessels. To achieve this, we correlated functional and structural barrier features to gene expression of endothelial cells (ECs) derived from different vascular beds. Within a subset of identified candidates, we found that the guanosine nucleotide exchange factor Vav3 was exclusively expressed by microvascular ECs and was closely associated with a high-resistance barrier phenotype. Ectopic expression of Vav3 in large artery and brain ECs significantly enhanced barrier resistance and cortical rearrangement of the actin cytoskeleton. Mechanistically, we found that the barrier effect of Vav3 is dependent on its Dbl homology domain and downstream activation of Rap1. Importantly, inactivation of Vav3 in vivo resulted in increased vascular leakage, highlighting its function as a key regulator of barrier stability.

scholarly journals IL33/ST2 Axis in Diabetic Kidney Disease: A Literature Review

Medicina ◽  
2019 ◽  
Vol 55 (2) ◽  
pp. 50 ◽  
Author(s):  
Alessandro Tonacci ◽  
Paolina Quattrocchi ◽  
Sebastiano Gangemi
Keyword(s):  
Kidney Disease ◽  
Literature Review ◽  
Diabetic Kidney Disease ◽  
Inflammatory Diseases ◽  
Th2 Cells ◽  
Renal Diseases ◽  
Diabetic Kidney ◽  
Interleukin 33 ◽  
Endothelial Barriers ◽  
Barrier Tissues

Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, playing a role in inflammatory, infectious and autoimmune diseases and expressed in the cellular nucleus in several tissues. High levels of IL-33 are expressed in epithelial barrier tissues and endothelial barriers. ST2 is a receptor for IL-33, expressed selectively on a subset of Th2 cells, mediating some of their functions. The IL-33/ST2 axis plays an important role in several acute and chronic inflammatory diseases, including asthma and rheumatoid arthritis. Different disorders are related to the activity of IL-33, ST2, or their axis, including cardiovascular disease or renal disturbances. Therefore, in the present work, a literature review was conducted, covering the period from 1 January 2000 to 30 November 2018, in PubMed, ScienceDirect, and Google Scholar database, to assess the involvement of the IL-33/ST2 axis in diabetic kidney disease. 6 articles directly dealing with the argument were identified, highlighting a clear link between IL-33/ST2 axis and diabetic kidney disease or related nephropathy. Overall, the involvement of ST2 seems to be more predictive than IL-33, especially in investigating the deterioration of kidney function; however, both compounds are pivotal in the field of renal diseases. Future studies are required to confirm the scientific evidences on larger and more heterogeneous cohorts.

scholarly journals Lymph node B lymphocyte trafficking is constrained by anatomy and highly dependent upon chemoattractant desensitization

Blood ◽  
2012 ◽  
Vol 119 (4) ◽  
pp. 978-989 ◽  
Author(s):  
Chung Park ◽  
Il-Young Hwang ◽  
Rajesh K. Sinha ◽  
Olena Kamenyeva ◽  
Michael D. Davis ◽  
...  
Keyword(s):  
Cell Migration ◽  
Lymph Node ◽  
B Cells ◽  
Lymph Nodes ◽  
B Cell ◽  
B Lymphocyte ◽  
Lymphocyte Trafficking ◽  
High Endothelial Venules ◽  
Endothelial Barriers ◽  
Basal Portion

Abstract B lymphocyte recirculation through lymph nodes (LNs) requires crossing endothelial barriers and chemoattractant-triggered cell migration. Here we show how LN anatomy and chemoattractant receptor signaling organize B lymphocyte LN trafficking. Blood-borne B cells predominately used CCR7 signaling to adhere to high endothelial venules (HEVs). New B cell emigrants slowly transited the HEV perivenule space, and thereafter localized nearby, avoiding the follicle. Eventually, the newly arrived B cells entered the basal portion of the follicle gradually populating it. In contrast, newly arriving activated B cells rapidly crossed HEVs and migrated toward the lymph node follicle. During their LN residency, recirculating B cells reacquired their sphingosine-1 phospate receptor 1 (S1P1) receptors and markedly attenuated their sensitivity to chemokines. Eventually, the B cells exited the LN follicle by entering the cortical lymphatics or returning to the paracortical cords. Upon entering the lymph, the B cells lost their polarity, down-regulated their S1P1 receptors, and subsequently strongly up-regulated their sensitivity to chemokines. These results are summarized in a model of homeostatic trafficking of B cells through LNs.

scholarly journals Cancer-Secreted miR-105 Destroys Vascular Endothelial Barriers to Promote Metastasis

Cancer Cell ◽  
2014 ◽  
Vol 25 (4) ◽  
pp. 501-515 ◽  
Author(s):  
Weiying Zhou ◽  
Miranda Y. Fong ◽  
Yongfen Min ◽  
George Somlo ◽  
Liang Liu ◽  
...  
Keyword(s):  
Vascular Endothelial ◽  
Endothelial Barriers
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