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Immunometabolism: From Molecular Mechanisms to Therapeutics
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Immunometabolism: From Molecular Mechanisms to Therapeutics

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: closed (30 June 2022) | Viewed by 8730

Special Issue Editor

Dr. Keiko Hosohata

E-Mail Website
Guest Editor
Education and Research Center for Clinical Pharmacy, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki 569-1094, Japan
Interests: inflammation; reactive oxygen species; renal physiology; blood pressure regulation; biomarker; clinical pharmacology; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is a worldwide epidemic, so it has become increasingly important to understand how metabolic imbalance drives various disease pathogeneses. Today, it is widely recognized that obesity impacts the immune system and that obesity-associated inflammation contributes to metabolic diseases, such as diabetes, cardiovascular disease, renal disease, and cancer.

This Special Issue of the International Journal of Molecular Sciences will focus on recent developments in the area of acute lung injury pathogenesis and treatment, including new insights into the mechanisms of and emerging therapies for immunology and metabolism, and will discuss the cell types, mediators, and pathways that contribute to immunological–metabolic crosstalk.

This Special Issue will gather reviews and original data that focus on defining the following:

  • Immunometabolism in macrophage polarization;
  • Metabolism for immune homeostasis in allergic diseases;
  • Glucose-mediated renal injury associated with a disruption in mitochondrial metabolic agility, inflammation, and fibrosis;
  • Cellular metabolism in ANCA vasculitis.

Dr. Keiko Hosohata
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

  • immunometabolism
  • immunotherapy
  • adipose tissue
  • inflammatory response
  • kidney disease
  • ANCA-associated vasculitis

Published Papers (3 papers)

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Research

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14 pages, 1487 KiB  
Article
LXRα Regulates oxLDL-Induced Trained Immunity in Macrophages
by Hannes M. Findeisen, Vivienne C. Voges, Laura C. Braun, Jannik Sonnenberg, Dennis Schwarz, Helena Körner, Holger Reinecke and Yahya Sohrabi
Int. J. Mol. Sci. 2022, 23(11), 6166; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23116166 - 31 May 2022
Cited by 17 | Viewed by 3549
Abstract
Reprogramming of metabolic pathways in monocytes and macrophages can induce a proatherosclerotic inflammatory memory called trained innate immunity. Here, we have analyzed the role of the Liver X receptor (LXR), a crucial regulator of metabolism and inflammation, in oxidized low-density lipoprotein (oxLDL)-induced trained [...] Read more.
Reprogramming of metabolic pathways in monocytes and macrophages can induce a proatherosclerotic inflammatory memory called trained innate immunity. Here, we have analyzed the role of the Liver X receptor (LXR), a crucial regulator of metabolism and inflammation, in oxidized low-density lipoprotein (oxLDL)-induced trained innate immunity. Human monocytes were incubated with LXR agonists, antagonists, and oxLDL for 24 h. After five days of resting time, cells were restimulated with the TLR-2 agonist Pam3cys. OxLDL priming induced the expression of LXRα but not LXRβ. Pharmacologic LXR activation was enhanced, while LXR inhibition prevented the oxLDL-induced inflammatory response. Furthermore, LXR inhibition blocked the metabolic changes necessary for epigenetic reprogramming associated with trained immunity. In fact, enrichment of activating histone marks at the IL-6 and TNFα promotor was reduced following LXR inhibition. Based on the differential expression of the LXR isoforms, we inhibited LXRα and LXRβ genes using siRNA in THP1 cells. As expected, siRNA-mediated knock-down of LXRα blocked the oxLDL-induced inflammatory response, while knock-down of LXRβ had no effect. We demonstrate a specific and novel role of the LXRα isoform in the regulation of oxLDL-induced trained immunity. Our data reveal important aspects of LXR signaling in innate immunity with relevance to atherosclerosis formation. Full article
(This article belongs to the Special Issue Immunometabolism: From Molecular Mechanisms to Therapeutics)
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7 pages, 1495 KiB  
Article
Glaucocalyxin A Ameliorates Hypoxia/Reoxygenation-Induced Injury in Human Renal Proximal Tubular Epithelial Cell Line HK-2 Cells
by Keiko Hosohata, Denan Jin and Shinji Takai
Int. J. Mol. Sci. 2022, 23(1), 446; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010446 - 31 Dec 2021
Cited by 5 | Viewed by 2109
Abstract
Ischemia-reperfusion injury is one of the major causes of acute kidney injury (AKI), which is increasingly prevalent in clinical settings. Glaucocalxin A (GLA), a biologically ent-kauranoid diterpenoid, has various pharmacological effects like antioxidation, immune regulation, and antiatherosclerosis. In this study, the effect of [...] Read more.
Ischemia-reperfusion injury is one of the major causes of acute kidney injury (AKI), which is increasingly prevalent in clinical settings. Glaucocalxin A (GLA), a biologically ent-kauranoid diterpenoid, has various pharmacological effects like antioxidation, immune regulation, and antiatherosclerosis. In this study, the effect of GLA on AKI and its mechanism were studied in vitro. HK-2 human renal tubular epithelial cells were exposed to hypoxia/reoxygenation (H/R), which were established as an in vitro AKI model. Subsequently, the mRNA expressions of inflammatory and antioxidant factors were determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Reactive oxygen species (ROS) production and cell death were detected by fluorescence-activated cell sorting. GLA pre-treatment improved the cell viability of HK-2 cells exposed to H/R. GLA suppressed the H/R-induced ROS production in HK-2 cells. GLA also elevated the activities of superoxide dismutase of HK-2 cells exposed to H/R. Moreover, GLA prevented H/R-induced cell death in HK-2 cells. Furthermore, GLA ameliorated the activation of the protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in HK-2 cells exposed to H/R. Our findings suggested that GLA protected HK-2 cells from H/R-induced oxidative damage, which was mediated by the Akt/Nrf2/HO-1 signaling pathway. These results indicate that GLA may serve as a promising therapeutic drug for AKI. Full article
(This article belongs to the Special Issue Immunometabolism: From Molecular Mechanisms to Therapeutics)
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Review

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15 pages, 329 KiB  
Review
SARS-CoV-2 Associated Immune Dysregulation and COVID-Associated Pulmonary Aspergilliosis (CAPA): A Cautionary Tale
by Dominic Adam Worku
Int. J. Mol. Sci. 2022, 23(6), 3228; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063228 - 17 Mar 2022
Cited by 3 | Viewed by 2223
Abstract
As the global SARS-CoV-2 pandemic continues to plague healthcare systems, it has become clear that opportunistic pathogens cause a considerable proportion of SARS-CoV-2-associated mortality and morbidity cases. Of these, Covid-Associated Pulmonary Aspergilliosis (CAPA) is a major concern with evidence that it occurs in [...] Read more.
As the global SARS-CoV-2 pandemic continues to plague healthcare systems, it has become clear that opportunistic pathogens cause a considerable proportion of SARS-CoV-2-associated mortality and morbidity cases. Of these, Covid-Associated Pulmonary Aspergilliosis (CAPA) is a major concern with evidence that it occurs in the absence of traditional risk factors such as neutropenia and is diagnostically challenging for the attending physician. In this review, we focus on the immunopathology of SARS-CoV-2 and how this potentiates CAPA through dysregulation of local and systemic immunity as well as the unintended consequences of approved COVID treatments including corticosteroids and IL-6 inhibitors. Finally, we will consider how knowledge of the above may aid in the diagnosis of CAPA using current diagnostics and what treatment should be instituted in probable and confirmed cases. Full article
(This article belongs to the Special Issue Immunometabolism: From Molecular Mechanisms to Therapeutics)
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