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Metabolic Regulation in Innate Immune Cells in Health and Disease
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Metabolic Regulation in Innate Immune Cells in Health and Disease

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

Deadline for manuscript submissions: 15 May 2024 | Viewed by 1859

Special Issue Editors

Dr. Yahya Sohrabi

E-Mail Website
Guest Editor
Department of Cardiology I—Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Münster, 48149 Münster, Germany
Interests: innate immunity; genetic susceptibility; inflammation; epigenetics; metabolism; trained immunity
Dr. Marc Dorenkamp

E-Mail Website
Guest Editor
Research Group Vascular Signalling, Universität Münster, 48149 Munster, Germany
Interests: cardiovascular; diabetes; monocytes; platelets; tyrosin phosphatase; hypertension; cardiovascular signaling; atherosclerosis; arteriogenesis; cell migration; heart failure; myocardial infarction; coronary heart disease; endothelial dysfunction

Special Issue Information

Dear Colleagues,

Current knowledge highlights the significant role of metabolic genes, transcription factors and regulatory enzymes in establishing chronic inflammation and aggravating the disease condition. The cellular metabolism is not only crucial for cellular processes, but it is also a hallmark for a disease’s condition. Metabolic pathways in innate immune cells contribute to host responses and the development of inflammation. Therefore, understanding the mechanisms that control cell metabolism in health and disease conditions can help identify new therapeutic targets or preventive strategies. In this Special Issue, we aim to collect research papers that are specifically focused on dissecting regulatory mechanisms of cell metabolism and metabolic changes in innate immune cells in vivo and in vitro.

Dr. Yahya Sohrabi
Dr. Marc Dorenkamp
Guest Editors

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

  • innate immunity
  • inflammation
  • epigenetics
  • metabolism
  • atherosclerosis
  • diabetes
  • obesity
  • liver diseases

Published Papers (1 paper)

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Research

20 pages, 3030 KiB  
Article
Tff3−/− Knock-Out Mice with Altered Lipid Metabolism Exhibit a Lower Level of Inflammation following the Dietary Intake of Sodium Chloride for One Week
by Nikolina Kolobarić, Martina Mihalj, Nataša Kozina, Anita Matić, Zrinka Mihaljević, Ivana Jukić and Ines Drenjančević
Int. J. Mol. Sci. 2023, 24(8), 7315; https://doi.org/10.3390/ijms24087315 - 15 Apr 2023
Cited by 1 | Viewed by 1391
Abstract
A high salt intake causes hemodynamic changes and promotes immune response through cell activation and cytokine production, leading to pro-inflammatory conditions. Transgenic Tff3−/− knock-out mice (TFF3ko) (n = 20) and wild-type mice (WT) (n = 20) were each divided into [...] Read more.
A high salt intake causes hemodynamic changes and promotes immune response through cell activation and cytokine production, leading to pro-inflammatory conditions. Transgenic Tff3−/− knock-out mice (TFF3ko) (n = 20) and wild-type mice (WT) (n = 20) were each divided into the (1) low-salt (LS) group and (2) high-salt (HS) group. Ten-week-old animals were fed with standard rodent chow (0.4% NaCl) (LS) or food containing 4% NaCl (HS) for one week (7 days). Inflammatory parameters from the sera were measured by Luminex assay. The integrin expression and rates of T cell subsets of interest from the peripheral blood leukocytes (PBLs) and mesenteric lymph nodes (MLNs) were measured using flow cytometry. There was a significant increase in high-sensitivity C reactive protein (hsCRP) only in the WT mice following the HS diet, while there were no significant changes in the serum levels of IFN-γ, TNF-α, IL-2, IL-4, or IL-6 as a response to treatment in either study groups. The rates of CD4+CD25+ T cells from MLNs decreased, while CD3+γδTCR+ from peripheral blood increased following the HS diet only in TFF3ko. γδTCR expressing T cell rates decreased in WT following the HS diet. The CD49d/VLA-4 expression decreased in the peripheral blood leukocytes in both groups following the HS diet. CD11a/LFA-1 expression significantly increased only in the peripheral blood Ly6C−CD11ahigh monocytes in WT mice following salt loading. In conclusion, salt-loading in knock-out mice caused a lower level of inflammatory response compared with their control WT mice due to gene depletion. Full article
(This article belongs to the Special Issue Metabolic Regulation in Innate Immune Cells in Health and Disease)
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