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Biological Barriers
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Biological Barriers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 20652

Special Issue Editor

Prof. Dr. Takaki Ishikawa

E-Mail Website1 Website2
Guest Editor
Department of Legal Medicine, Osaka City University Medical School, 1-4-3 Asahi-machi, Abeno, Osaka 545-8585, Japan
Interests: forensic science; forensic pathology; toxicology; biochemistry; endocrinology and metabolism

Special Issue Information

Dear Colleagues,

International Journal of Molecular Sciences (ISSN 1422-0067, IF 4.556) is currently running a Special Issue focused on "Biological Barriers". Prof. Takaki Ishikawa is serving as Guest Editor for this issue. Based on your excellent expertise, we would be thrilled if you could submit a paper to this issue.

The natural existence of different biological barriers plays a very important role in the function and integrity of numerous vertebrate organs. Biological barriers are living organisms that help to protect the body from pathogens. On the other hand, biological barriers are known to have an inverse relationship between concentrations of the drugs in plasma and the efficacy of the drug. Overcoming biological barriers, including skin, mucosal membranes, the blood–brain barrier, as well as cell and nuclear membranes, constitutes a key hurdle in the field of drug delivery. While these barriers serve a natural protective function in the body, they limit delivery of drugs into the body.

This Special Issue focuses on the study of the biochemistry, molecular biology and physiology of these biological barriers. Potential topics include but are not limited to the molecular mechanisms involved in biological barriers (including skin, mucosal membranes, the blood–brain barrier, as well as cell and nuclear membranes) alteration and breakdown in immunoreaction and pathophysiology; drug delivery across biological barriers in relation to delivery systems that facilitate the transport of drug-containing nanosystems at the tissue, cell, and subcellular levels. We warmly welcome original papers and reviews on this widely discussed topic.

Prof. Dr. Takaki Ishikawa
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • biological barriers
  • blood–brain barrier
  • mucosal membranes
  • gastrointestinal barrier
  • phagocytic cells
  • cancer microenvironment
  • drug delivery
  • drug transport across the barriers

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Published Papers (6 papers)

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Research

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19 pages, 9438 KiB  
Article
Uptake of Tropheryma whipplei by Intestinal Epithelia
by Julian Friebel, Katina Schinnerling, Kathleen Weigt, Claudia Heldt, Anja Fromm, Christian Bojarski, Britta Siegmund, Hans-Jörg Epple, Judith Kikhney, Annette Moter, Thomas Schneider, Jörg D. Schulzke, Verena Moos and Michael Schumann
Int. J. Mol. Sci. 2023, 24(7), 6197; https://doi.org/10.3390/ijms24076197 - 24 Mar 2023
Cited by 1 | Viewed by 2943
Abstract
Background: Tropheryma whipplei (TW) can cause different pathologies, e.g., Whipple’s disease and transient gastroenteritis. The mechanism by which the bacteria pass the intestinal epithelial barrier, and the mechanism of TW-induced gastroenteritis are currently unknown. Methods: Using ex vivo disease models [...] Read more.
Background: Tropheryma whipplei (TW) can cause different pathologies, e.g., Whipple’s disease and transient gastroenteritis. The mechanism by which the bacteria pass the intestinal epithelial barrier, and the mechanism of TW-induced gastroenteritis are currently unknown. Methods: Using ex vivo disease models comprising human duodenal mucosa exposed to TW in Ussing chambers, various intestinal epithelial cell (IEC) cultures exposed to TW and a macrophage/IEC coculture model served to characterize endocytic uptake mechanisms and barrier function. Results: TW exposed ex vivo to human small intestinal mucosae is capable of autonomously entering IECs, thereby invading the mucosa. Using dominant-negative mutants, TW uptake was shown to be dynamin- and caveolin-dependent but independent of clathrin-mediated endocytosis. Complementary inhibitor experiments suggested a role for the activation of the Ras/Rac1 pathway and actin polymerization. TW-invaded IECs underwent apoptosis, thereby causing an epithelial barrier defect, and were subsequently subject to phagocytosis by macrophages. Conclusions: TW enters epithelia via an actin-, dynamin-, caveolin-, and Ras-Rac1-dependent endocytosis mechanism and consecutively causes IEC apoptosis primarily in IECs invaded by multiple TW bacteria. This results in a barrier leak. Moreover, we propose that TW-packed IECs can be subject to phagocytic uptake by macrophages, thereby opening a potential entry point of TW into intestinal macrophages. Full article
(This article belongs to the Special Issue Biological Barriers)
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14 pages, 3066 KiB  
Article
Self-Assembled Daunorubicin/Epigallocatechin Gallate Nanocomplex for Synergistic Reversal of Chemoresistance in Leukemia
by Ki Hyun Bae, Fritz Lai, Betul Oruc, Motomi Osato, Qingfeng Chen and Motoichi Kurisawa
Int. J. Mol. Sci. 2023, 24(1), 381; https://doi.org/10.3390/ijms24010381 - 26 Dec 2022
Cited by 7 | Viewed by 2383
Abstract
Chemoresistance is one of the major challenges for the treatment of acute myeloid leukemia. Epigallocatechin gallate (EGCG), a bioactive polyphenol from green tea, has attracted immense interest as a potential chemosensitizer, but its application is limited due to the need for effective formulations [...] Read more.
Chemoresistance is one of the major challenges for the treatment of acute myeloid leukemia. Epigallocatechin gallate (EGCG), a bioactive polyphenol from green tea, has attracted immense interest as a potential chemosensitizer, but its application is limited due to the need for effective formulations capable of co-delivering EGCG and anti-leukemic drugs. Herein, we describe the formation and characterization of a micellar nanocomplex self-assembled from EGCG and daunorubicin, an anthracycline drug for the first-line treatment of acute myeloid leukemia. This nanocomplex was highly stable at pH 7.4 but stimulated to release the incorporated daunorubicin at pH 5.5, mimicking an acidic endosomal environment. More importantly, the nanocomplex exhibited superior cytotoxic efficacy against multidrug-resistant human leukemia cells over free daunorubicin by achieving a strong synergism, as supported by median-effect plot analysis. The observed chemosensitizing effect was in association with enhanced nucleus accumulation of daunorubicin, elevation of intracellular reactive oxygen species and caspase-mediated apoptosis induction. Our study presents a promising strategy for circumventing chemoresistance for more effective leukemia therapy. Full article
(This article belongs to the Special Issue Biological Barriers)
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15 pages, 2505 KiB  
Article
Different Involvement of Vimentin during Invasion by Listeria monocytogenes at the Blood–Brain and the Blood–Cerebrospinal Fluid Barriers In Vitro
by Franjo Banovic, Sandrin Schulze, Mobarak Abu Mraheil, Torsten Hain, Trinad Chakraborty, Véronique Orian-Rousseau, Selina Moroniak, Christel Weiss, Hiroshi Ishikawa, Horst Schroten, Rüdiger Adam and Christian Schwerk
Int. J. Mol. Sci. 2022, 23(21), 12908; https://doi.org/10.3390/ijms232112908 - 26 Oct 2022
Cited by 3 | Viewed by 2634
Abstract
The human central nervous system (CNS) is separated from the blood by distinct cellular barriers, including the blood–brain barrier (BBB) and the blood–cerebrospinal fluid (CFS) barrier (BCSFB). Whereas at the center of the BBB are the endothelial cells of the brain capillaries, the [...] Read more.
The human central nervous system (CNS) is separated from the blood by distinct cellular barriers, including the blood–brain barrier (BBB) and the blood–cerebrospinal fluid (CFS) barrier (BCSFB). Whereas at the center of the BBB are the endothelial cells of the brain capillaries, the BCSFB is formed by the epithelium of the choroid plexus. Invasion of cells of either the BBB or the BCSFB is a potential first step during CNS entry by the Gram-positive bacterium Listeria monocytogenes (Lm). Lm possesses several virulence factors mediating host cell entry, such as the internalin protein family—including internalin (InlA), which binds E-cadherin (Ecad) on the surface of target cells, and internalin B (InlB)—interacting with the host cell receptor tyrosine kinase Met. A further family member is internalin (InlF), which targets the intermediate filament protein vimentin. Whereas InlF has been shown to play a role during brain invasion at the BBB, its function during infection at the BCSFB is not known. We use human brain microvascular endothelial cells (HBMEC) and human choroid plexus epithelial papilloma (HIBCPP) cells to investigate the roles of InlF and vimentin during CNS invasion by Lm. Whereas HBMEC present intracellular and surface vimentin (besides Met), HIBCPP cells do not express vimentin (except Met and Ecad). Treatment with the surface vimentin modulator withaferin A (WitA) inhibited invasion of Lm into HBMEC, but not HIBCPP cells. Invasion of Lm into HBMEC and HIBCPP cells is, however, independent of InlF, since a deletion mutant of Lm lacking InlF did not display reduced invasion rates. Full article
(This article belongs to the Special Issue Biological Barriers)
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8 pages, 1489 KiB  
Article
Anti-Inflammatory Effect of Sparstolonin B through Inhibiting Expression of NF-κB and STAT-1
by Nayeon Kim, Chaeyeong Kim, Soo Ho Ryu, Go Oun Kim and Jong-Sup Bae
Int. J. Mol. Sci. 2022, 23(18), 10213; https://doi.org/10.3390/ijms231810213 - 6 Sep 2022
Cited by 5 | Viewed by 2098
Abstract
Sparstolonin B (SsnB), which is found in Sparganium stoloniferum, prevents the synthesis of inflammatory mediators and is related to functional pathways of survival. In this study, we assessed the possible protective functions of SsnB on lipopolysaccharide (LPS)-induced inflammatory responses. We determined the functions [...] Read more.
Sparstolonin B (SsnB), which is found in Sparganium stoloniferum, prevents the synthesis of inflammatory mediators and is related to functional pathways of survival. In this study, we assessed the possible protective functions of SsnB on lipopolysaccharide (LPS)-induced inflammatory responses. We determined the functions of SsnB on controlling heme oxygenase (HO)-1, cyclooxygenase (COX-)2, and inducible nitric oxide synthase (iNOS) in LPS-activated human umbilical vein endothelial cells (HUVECs). Furthermore, the distinct function of SsnB on the expression of iNOS and well-known pro-inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, were assessed in the pulmonary histological status of LPS-injected mice. SsnB upregulated the HO-1 production, inhibited luciferase-NF-κB interaction, and lowered COX-2/PGE2 and iNOS/NO, which lead to the reduction of STAT-1 phosphorylation. Moreover, SsnB enhanced the nuclear translocation of Nrf2, elevated the binding activity between Nrf2 and antioxidant response elements (AREs), and weakened IL-1β expression on LPS-treated HUVECs. SsnB-suppressed iNOS/NO synthesis was restored by the process of the RNAi inhibition of HO-1. In experiment with an LPS-injected animal model, SsnB remarkably decreased the iNOS expression in the pulmonary biostructure and TNF-α level in the bronchoalveolar lavage fluid (BALF). Therefore, these results demonstrate that SsnB is responsible for inflammation ameliorative activity by controlling iNOS through inhibition of both NF-κB expression and p-STAT-1. Therefore, SsnB could be a candidate for promoting novel clinical substances to remedy pathologic inflammation. Full article
(This article belongs to the Special Issue Biological Barriers)
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Review

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23 pages, 1525 KiB  
Review
Neurogenic Hypertension, the Blood–Brain Barrier, and the Potential Role of Targeted Nanotherapeutics
by Richard Nii Lante Lamptey, Chengwen Sun, Buddhadev Layek and Jagdish Singh
Int. J. Mol. Sci. 2023, 24(3), 2213; https://doi.org/10.3390/ijms24032213 - 22 Jan 2023
Cited by 12 | Viewed by 5216
Abstract
Hypertension is a major health concern globally. Elevated blood pressure, initiated and maintained by the brain, is defined as neurogenic hypertension (NH), which accounts for nearly half of all hypertension cases. A significant increase in angiotensin II-mediated sympathetic nervous system activity within the [...] Read more.
Hypertension is a major health concern globally. Elevated blood pressure, initiated and maintained by the brain, is defined as neurogenic hypertension (NH), which accounts for nearly half of all hypertension cases. A significant increase in angiotensin II-mediated sympathetic nervous system activity within the brain is known to be the key driving force behind NH. Blood pressure control in NH has been demonstrated through intracerebrovascular injection of agents that reduce the sympathetic influence on cardiac functions. However, traditional antihypertensive agents lack effective brain permeation, making NH management extremely challenging. Therefore, developing strategies that allow brain-targeted delivery of antihypertensives at the therapeutic level is crucial. Targeting nanotherapeutics have become popular in delivering therapeutics to hard-to-reach regions of the body, including the brain. Despite the frequent use of nanotherapeutics in other pathological conditions such as cancer, their use in hypertension has received very little attention. This review discusses the underlying pathophysiology and current management strategies for NH, as well as the potential role of targeted therapeutics in improving current treatment strategies. Full article
(This article belongs to the Special Issue Biological Barriers)
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15 pages, 900 KiB  
Review
T Cell Subsets and Natural Killer Cells in the Pathogenesis of Nonalcoholic Fatty Liver Disease
by Yoseph Asmelash Gebru, Haripriya Gupta, Hyeong Seop Kim, Jung A. Eom, Goo Hyun Kwon, Eunju Park, Jin-Ju Jeong, Sung-Min Won, Satya Priya Sharma, Raja Ganesan, Dong Joon Kim and Ki Tae Suk
Int. J. Mol. Sci. 2021, 22(22), 12190; https://doi.org/10.3390/ijms222212190 - 11 Nov 2021
Cited by 25 | Viewed by 4391
Abstract
Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by hepatic accumulation of excess lipids. T cells are commonly classified into various subsets based on their surface markers including T cell receptors, type of antigen presentation and pathophysiological functions. Several studies have implicated [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by hepatic accumulation of excess lipids. T cells are commonly classified into various subsets based on their surface markers including T cell receptors, type of antigen presentation and pathophysiological functions. Several studies have implicated various T cell subsets and natural killer (NK) cells in the progression of NAFLD. While NK cells are mainly components of the innate hepatic immune system, the majority of T cell subsets can be part of both the adaptive and innate systems. Several studies have reported that various stages of NAFLD are accompanied by the accumulation of distinct T cell subsets and NK cells with different functions and phenotypes observed usually resulting in proinflammatory effects. More importantly, the overall stimulation of the intrahepatic T cell subsets is directly influenced by the homeostasis of the gut microbiota. Similarly, NK cells have been found to accumulate in the liver in response to pathogens and tumors. In this review, we discussed the nature and pathophysiological roles of T cell subsets including γδ T cells, NKT cells, Mucosal-associated invariant T (MAIT) cells as well as NK cells in NAFLD. Full article
(This article belongs to the Special Issue Biological Barriers)
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