Leukocyte-Endothelial Interactions within the Microcirculation

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 2137

Special Issue Editor


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Dear Colleagues,

Leukocyte–endothelial interactions within microcirculation are crucial to maintaining homeostasis under physiological conditions and are considered the “battlefield” of the immune response during inflammation and infection. For this Special Issue of “Biomedicines”, we encourage the contribution of papers reflecting basic science and clinical microcirculation research describing the behavior of leukocytes and their counterpart, endothelial cells, in different microvascular beds with regard to health and disease. In particular, translational research in animal models is welcomed, from observational studies to mechanistic approaches, including experimental pharmacological treatments and genetic experiments.  

Prof. Dr. Christian Lehmann
Guest Editor

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Keywords

  • leukocytes
  • endothelial cells
  • microcirculation
  • immunity
  • inflammation

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Published Papers (2 papers)

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Research

11 pages, 2140 KiB  
Article
The Hydroxypyridinone Iron Chelator DIBI Reduces Bacterial Load and Inflammation in Experimental Lung Infection
by Xiyang Zhang, Rhea Nickerson, Lauren Burton, Ashley Stueck, Bruce Holbein, Zhenyu Cheng, Juan Zhou and Christian Lehmann
Biomedicines 2024, 12(7), 1452; https://doi.org/10.3390/biomedicines12071452 - 29 Jun 2024
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Abstract
Iron plays a critical role in lung infections due to its function in the inflammatory immune response but also as an important factor for bacterial growth. Iron chelation represents a potential therapeutic approach to inhibit bacterial growth and pathologically increased pro-inflammatory mediator production. [...] Read more.
Iron plays a critical role in lung infections due to its function in the inflammatory immune response but also as an important factor for bacterial growth. Iron chelation represents a potential therapeutic approach to inhibit bacterial growth and pathologically increased pro-inflammatory mediator production. The present study was designed to investigate the impact of the iron chelator DIBI in murine lung infection induced by intratracheal Pseudomonas aeruginosa (strain PA14) administration. DIBI is a polymer with a polyvinylpyrrolidone backbone containing nine 3-hydroxy-1-(methacrylamidoethyl)-2-methyl-4(1H) pyridinone (MAHMP) residues per molecule and was given by intraperitoneal injection either as a single dose (80 mg/kg) immediately after PA14 administration or a double dose (second dose 4 h after PA14 administration). The results showed that lung NF-κBp65 levels, as well as levels of various inflammatory cytokines (TNFα, IL-1β, IL-6) both in lung tissue and bronchoalveolar lavage fluid (BALF), were significantly increased 24 h after PA14 administration. Single-dose DIBI did not affect the bacterial load or inflammatory response in the lungs or BALF. However, two doses of DIBI significantly decreased bacterial load, attenuated NF-κBp65 upregulation, reduced inflammatory cytokines production, and relieved lung tissue damage. Our findings support the conclusion that the iron chelator, DIBI, can reduce lung injury induced by P. aeruginosa, via its anti-bacterial and anti-inflammatory effects. Full article
(This article belongs to the Special Issue Leukocyte-Endothelial Interactions within the Microcirculation)
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13 pages, 1316 KiB  
Article
Understanding Local Reactions Induced by Bothrops jararaca Venom: The Role of Inflammatory Mediators in Leukocyte–Endothelium Interactions
by Bianca Cestari Zychar and Luís Roberto C. Gonçalves
Biomedicines 2024, 12(4), 734; https://doi.org/10.3390/biomedicines12040734 - 26 Mar 2024
Cited by 1 | Viewed by 1115
Abstract
In recent years, extensive research has delved into the pathophysiology of local reactions triggered by Bothrops snake venoms. Even though antivenom works well at reducing death and systemic effects, it is still not very effective in treating local reactions because it cannot counteract [...] Read more.
In recent years, extensive research has delved into the pathophysiology of local reactions triggered by Bothrops snake venoms. Even though antivenom works well at reducing death and systemic effects, it is still not very effective in treating local reactions because it cannot counteract damage that has already been triggered. This limitation might be attributed to certain molecules that amplify the venom-induced innate response. While evidence suggests endogenous mediators at the venom site play a role in this envenomation, in Brazil, the concurrent use of anti-inflammatory agents or other drugs alongside antivenom remains uncommon. This study evaluated the pharmacological mediation of alterations in leukocyte–endothelium interactions following the experimental envenomation of mice with Bothrops jararaca venom, the main culprit of snake-related accidents in Southeast Brazil. We treated envenomed mice with inhibitors of different pharmacological pathways and observed the cremaster muscle microcirculation with intravital microscopy. We found that eicosanoids related to cyclooxygenase pathways and nitric oxide significantly contributed to B. jararaca venom-induced alterations in leukocyte–endothelium interactions. Conversely, lipoxygenase-mediated eicosanoids, histamine, and serotonin had minimal participation. Notably, dexamethasone and antivenom treatment diminished B. jararaca venom–induced alterations in leukocyte–endothelium interactions. The limited efficacy of the antivenom in managing Bothrops venom-induced local reactions emphasizes the critical need for supplementary treatments to enhance therapeutic outcomes. Full article
(This article belongs to the Special Issue Leukocyte-Endothelial Interactions within the Microcirculation)
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