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Cells
Special Issues
Endothelial Inflammation during Microbial Infections and Other Human Ailments
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Endothelial Inflammation during Microbial Infections and Other Human Ailments

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 4424

Special Issue Editor

Dr. Abha Sahni

E-Mail Website
Guest Editor
Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, TX, USA
Interests: intracellular bacteria; endothelium; infection; pathogenesis; host-pathogen interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The vascular endothelium plays a central role in the modulation of blood vessel function by regulating vascular tone, inflammation, and hemostasis. The onset of acute inflammation requires ‘endothelial activation’ to initiate the interactions between circulating immune cells and the monolayer of the endothelium. Now dubbed as conditional immune cells, endothelial cells trigger a rapid response to infectious microbes or injured tissues and recruit inflammatory immune cells to the loci of infection or tissue damage to eradicate invading microbes and to remove cellular debris. Thus, the vascular endothelium is directly involved in the pathogenesis of a broad spectrum of human ailments, including peripheral vascular disease, stroke, heart disease, diabetes, chronic kidney failure, tumor growth, metastasis, venous thrombosis, endometriosis, and, most importantly, infectious diseases. In this regard, recent studies implicated endothelial dysfunction and endotheliitis in the pathophysiology of COVID-19. Continued efforts to enhance our understanding of the roles of endothelial inflammation and associated processes during infection and other pathological disorders are likely to advance treatment options and preventative strategies for many human diseases. The aim of this Special Issue is to facilitate a compendium of exciting novel ideas on all aspects of endothelial activation and inflammation, in relation to infections and other human aliments.

Assoc. Prof. Dr. Abha Sahni
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • endothelium
  • inflammation
  • infection
  • human diseases
  • microbes
  • vascular remodeling
  • coagulation

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Published Papers (1 paper)

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Research

21 pages, 4263 KiB  
Article
Porphyromonas gingivalis Induces Proinflammatory Cytokine Expression Leading to Apoptotic Death through the Oxidative Stress/NF-κB Pathway in Brain Endothelial Cells
by Vichuda Charoensaensuk, Yen-Chou Chen, Yun-Ho Lin, Keng-Liang Ou, Liang-Yo Yang and Dah-Yuu Lu
Cells 2021, 10(11), 3033; https://doi.org/10.3390/cells10113033 - 5 Nov 2021
Cited by 20 | Viewed by 3897
Abstract
Porphyromonas gingivalis, a periodontal pathogen, has been proposed to cause blood vessel injury leading to cerebrovascular diseases such as stroke. Brain endothelial cells compose the blood-brain barrier that protects homeostasis of the central nervous system. However, whether P. gingivalis causes the death [...] Read more.
Porphyromonas gingivalis, a periodontal pathogen, has been proposed to cause blood vessel injury leading to cerebrovascular diseases such as stroke. Brain endothelial cells compose the blood-brain barrier that protects homeostasis of the central nervous system. However, whether P. gingivalis causes the death of endothelial cells and the underlying mechanisms remain unclear. This study aimed to investigate the impact and regulatory mechanisms of P. gingivalis infection in brain endothelial cells. We used bEnd.3 cells and primary mouse endothelial cells to assess the effects of P. gingivalis on endothelial cells. Our results showed that infection with live P. gingivalis, unlike heat-killed P. gingivalis, triggers brain endothelial cell death by inducing cell apoptosis. Moreover, P. gingivalis infection increased intracellular reactive oxygen species (ROS) production, activated NF-κB, and up-regulated the expression of IL-1β and TNF-α. Furthermore, N-acetyl-L-cysteine (NAC), a most frequently used antioxidant, treatment significantly reduced P. gingivalis-induced cell apoptosis and brain endothelial cell death. The enhancement of ROS production, NF-κB p65 activation, and proinflammatory cytokine expression was also attenuated by NAC treatment. The impact of P. gingivalis on brain endothelial cells was also confirmed using adult primary mouse brain endothelial cells (MBECs). In summary, our results showed that P. gingivalis up-regulates IL-1β and TNF-α protein expression, which consequently causes cell death of brain endothelial cells through the ROS/NF-κB pathway. Our results, together with the results of previous case-control studies and epidemiologic reports, strongly support the hypothesis that periodontal infection increases the risk of developing cerebrovascular disease. Full article
(This article belongs to the Special Issue Endothelial Inflammation during Microbial Infections and Other Human Ailments)
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