Inflammation in Target Organs

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

Deadline for manuscript submissions: 29 August 2024 | Viewed by 2380

Special Issue Editors


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Guest Editor
Diabetes Unit, The Faculty of Medicine, Department of Endocrinology and Metabolism, Hadassah Medical Center, Hebrew University of Jerusalem, Jerusalem 91120, Israel
Interests: insulin resistance; diabetes; lipid metabolism; glucose metabolism; disease prevention; obesity metabolic endocrinology; high fructose corn syrup; cardiovascular disease; obesity; telemedicine; telehealth; eHealth; mHealth; digital health; review; connected diabetes care; diabetes mellitus; glucose monitoring
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Guest Editor Assistant
Goldman Medical School, Faculty of Health Sciences, Ben Gurion University, Beer Sheva 8410501, Israel
Interests: diabetes; obesity
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Special Issue Information

Dear Colleagues,

Various metabolic disorders affect target organs, such as the heart, kidneys, liver, blood vessels, and the brain. A substantial portion of the resultant damage can be attributed to inflammatory processes, compromising the functionality of these organs. Inflammation may induce organ fibrosis and precipitate irreversible damage. In this Special Issue, we will present an overview elucidating the inflammatory response, resultant damage, and future therapies to prevent and cure inflammation in target organs. We will explore the intricate relationship between inflammation and organ damage, drawing insights from studies on cell lines, animal models, and humans.

This Special Issue endeavors to underscore recent discoveries, elucidating the intricate mechanisms through which inflammation inflicts damage on the target organs. Its objective is to offer a comprehensive scope, encompassing research papers and reviews delineating specific interactions between target organs and inflammation. Such discernments possess the potential to profoundly shape future therapeutic strategies within this domain of study.

Prof. Dr. Itamar Raz
Guest Editor

Roni Weinberg Sibony
Guest Editor Assistant

Manuscript Submission Information

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Keywords

  • inflammation
  • fibrosis
  • cardio-renal
  • vascular
  • liver
  • brain

Published Papers (2 papers)

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Research

16 pages, 4382 KiB  
Article
Combined Insults of a MASH Diet and Alcohol Binges Activate Intercellular Communication and Neutrophil Recruitment via the NLRP3-IL-1β Axis in the Liver
by Mrigya Babuta, Prashanth Thevkar Nagesh, Aditi Ashish Datta, Victoria Remotti, Yuan Zhuang, Jeeval Mehta, Francesca Lami, Yanbo Wang and Gyongyi Szabo
Cells 2024, 13(11), 960; https://doi.org/10.3390/cells13110960 - 1 Jun 2024
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Abstract
Binge drinking in obese patients positively correlates with accelerated liver damage and liver-related death. However, the underlying mechanism and the effect of alcohol use on the progression of metabolic-dysfunction-associated steatotic liver disease (MASLD) remain unexplored. Here, we show that short-term feeding of a [...] Read more.
Binge drinking in obese patients positively correlates with accelerated liver damage and liver-related death. However, the underlying mechanism and the effect of alcohol use on the progression of metabolic-dysfunction-associated steatotic liver disease (MASLD) remain unexplored. Here, we show that short-term feeding of a metabolic-dysfunction-associated steatohepatitis (MASH) diet plus daily acute alcohol binges for three days induce liver injury and activation of the NLRP3 inflammasome. We identify that a MASH diet plus acute alcohol binges promote liver inflammation via increased infiltration of monocyte-derived macrophages, neutrophil recruitment, and NET release in the liver. Our results suggest that both monocyte-derived macrophages and neutrophils are activated via NLRP3, while the administration of MCC950, an NLRP3 inhibitor, dampens these effects.In this study, we reveal important intercellular communication between hepatocytes and neutrophils. We discover that the MASH diet plus alcohol induces IL-1β via NLRP3 activation and that IL-1β acts on hepatocytes and promotes the production of CXCL1 and LCN2. In turn, the increase in these neutrophils recruits chemokines and causes further infiltration and activation of neutrophils in the liver. In vivo administration of the NLRP3 inhibitor, MCC950, improves the early phase of MetALD by preventing liver damage, steatosis, inflammation, and immune cells recruitment. Full article
(This article belongs to the Special Issue Inflammation in Target Organs)
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20 pages, 10992 KiB  
Article
Investigation into Cardiac Myhc-α 334–352-Specific TCR Transgenic Mice Reveals a Role for Cytotoxic CD4 T Cells in the Development of Cardiac Autoimmunity
by Meghna Sur, Mahima T. Rasquinha, Kiruthiga Mone, Chandirasegaran Massilamany, Ninaad Lasrado, Channabasavaiah Gurumurthy, Raymond A. Sobel and Jay Reddy
Cells 2024, 13(3), 234; https://doi.org/10.3390/cells13030234 - 26 Jan 2024
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Abstract
Myocarditis is one of the major causes of heart failure in children and young adults and can lead to dilated cardiomyopathy. Lymphocytic myocarditis could result from autoreactive CD4+ and CD8+ T cells, but defining antigen specificity in disease pathogenesis is challenging. [...] Read more.
Myocarditis is one of the major causes of heart failure in children and young adults and can lead to dilated cardiomyopathy. Lymphocytic myocarditis could result from autoreactive CD4+ and CD8+ T cells, but defining antigen specificity in disease pathogenesis is challenging. To address this issue, we generated T cell receptor (TCR) transgenic (Tg) C57BL/6J mice specific to cardiac myosin heavy chain (Myhc)-α 334–352 and found that Myhc-α-specific TCRs were expressed in both CD4+ and CD8+ T cells. To investigate if the phenotype is more pronounced in a myocarditis-susceptible genetic background, we backcrossed with A/J mice. At the fourth generation of backcrossing, we observed that Tg T cells from naïve mice responded to Myhc-α 334–352, as evaluated by proliferation assay and carboxyfluorescein succinimidyl ester staining. The T cell responses included significant production of mainly pro-inflammatory cytokines, namely interferon (IFN)-γ, interleukin-17, and granulocyte macrophage-colony stimulating factor. While the naïve Tg mice had isolated myocardial lesions, immunization with Myhc-α 334–352 led to mild myocarditis, suggesting that further backcrossing to increase the percentage of A/J genome close to 99.99% might show a more severe disease phenotype. Further investigations led us to note that CD4+ T cells displayed the phenotype of cytotoxic T cells (CTLs) akin to those of conventional CD8+ CTLs, as determined by the expression of CD107a, IFN-γ, granzyme B natural killer cell receptor (NKG)2A, NKG2D, cytotoxic and regulatory T cell molecules, and eomesodermin. Taken together, the transgenic system described in this report may be a helpful tool to distinguish the roles of cytotoxic cardiac antigen-specific CD4+ T cells vs. those of CD8+ T cells in the pathogenesis of myocarditis. Full article
(This article belongs to the Special Issue Inflammation in Target Organs)
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