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Metabolic Pathways in Immune Cells during Diseases
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Metabolic Pathways in Immune Cells during Diseases

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 November 2022) | Viewed by 19447

Special Issue Editors

Dr. Carmelo Luci

E-Mail Website
Guest Editor
Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte D’Azur, INSERM, 06204 Nice, France
Interests: innate lymphoid cells; inflammation and liver complications associated with obesity and alcohol; immunometabolism
Dr. Stoyan Ivanov

E-Mail Website
Guest Editor
Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte D’Azur, INSERM, 06204 Nice, France
Interests: monocytes; macrophages; dendritic cell and immunometabolism

Special Issue Information

Dear Colleagues, 

Immune cells are the gatekeepers of our body, and their functions are tightly regulated in order to achieve this role. Various innate and adaptive immune cell subsets have been described, and their specific contribution during cancer and infectious diseases, but also in the regulation of inflammation, has been illustrated. Over the past few years, the importance of nutrients and energy metabolism in regulating immune cell function has led to the emergence of a new field in immunology termed “immunometabolism”.

Cellular metabolism is indispensable for the activation and specialized functions of immune cells. How metabolic pathways are regulated by intrinsic and extrinsic signals to ensure a productive immune response is a major field of interest. In this Special Issue of IJMS, we hope that the entire scientific community will find and learn more about new advances in the field of immunometabolism. This collection will include aspects of how metabolism modulates the functions of innate and adaptive immune cells during various diseases (cancer, infection, metabolic disorders, and so on) and how the environment is involved in the metabolic reprogramming of these cells. Our aim for this Special Issue is to propose a collective work to seek novel research opportunities in the field of immunometabolism or review articles focused on the keywords listed below and dedicated to enhancing our understanding of disease progression, as well as having an impact on fundamental biology.

Dr. Carmelo Luci
Dr. Stoyan Ivanov
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 and adaptive immune cells
  • inflammation
  • metabolic diseases
  • pathogen infection
  • cancer
  • glycolysis
  • oxidative phosphorylation
  • fatty acid oxidation
  • amino acid metabolism
  • tricarboxylic acid cycle

Published Papers (4 papers)

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Research

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19 pages, 7867 KiB  
Article
Characterization of Early and Late Damage in a Mouse Model of Pelvic Radiation Disease
by Roberta Vitali, Francesca Palone, Ilaria De Stefano, Chiara Fiorente, Flavia Novelli, Emanuela Pasquali, Emiliano Fratini, Mirella Tanori, Simona Leonardi, Barbara Tanno, Eleonora Colantoni, Sara Soldi, Serena Galletti, Maria Grimaldi, Alessio Giuseppe Morganti, Lorenzo Fuccio, Simonetta Pazzaglia, Claudio Pioli, Mariateresa Mancuso and Loredana Vesci
Int. J. Mol. Sci. 2023, 24(10), 8800; https://doi.org/10.3390/ijms24108800 - 15 May 2023
Cited by 1 | Viewed by 1990
Abstract
Pelvic radiation disease (PRD), a frequent side effect in patients with abdominal/pelvic cancers treated with radiotherapy, remains an unmet medical need. Currently available preclinical models have limited applications for the investigation of PRD pathogenesis and possible therapeutic strategies. In order to select the [...] Read more.
Pelvic radiation disease (PRD), a frequent side effect in patients with abdominal/pelvic cancers treated with radiotherapy, remains an unmet medical need. Currently available preclinical models have limited applications for the investigation of PRD pathogenesis and possible therapeutic strategies. In order to select the most effective irradiation protocol for PRD induction in mice, we evaluated the efficacy of three different locally and fractionated X-ray exposures. Using the selected protocol (10 Gy/day × 4 days), we assessed PRD through tissue (number and length of colon crypts) and molecular (expression of genes involved in oxidative stress, cell damage, inflammation, and stem cell markers) analyses at short (3 h or 3 days after X-ray) and long (38 days after X-rays) post-irradiation times. The results show that a primary damage response in term of apoptosis, inflammation, and surrogate markers of oxidative stress was found, thus determining a consequent impairment of cell crypts differentiation and proliferation as well as a local inflammation and a bacterial translocation to mesenteric lymph nodes after several weeks post-irradiation. Changes were also found in microbiota composition, particularly in the relative abundance of dominant phyla, related families, and in alpha diversity indices, as an indication of dysbiotic conditions induced by irradiation. Fecal markers of intestinal inflammation, measured during the experimental timeline, identified lactoferrin, along with elastase, as useful non-invasive tools to monitor disease progression. Thus, our preclinical model may be useful to develop new therapeutic strategies for PRD treatment. Full article
(This article belongs to the Special Issue Metabolic Pathways in Immune Cells during Diseases)
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26 pages, 5568 KiB  
Article
Altered Fatty Acid Oxidation in Lymphocyte Populations of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
by Jessica Maya, Sabrina M. Leddy, C. Gunnar Gottschalk, Daniel L. Peterson and Maureen R. Hanson
Int. J. Mol. Sci. 2023, 24(3), 2010; https://doi.org/10.3390/ijms24032010 - 19 Jan 2023
Cited by 8 | Viewed by 9277
Abstract
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disabling multisystem illness in which individuals are plagued with fatigue, inflammatory symptoms, cognitive dysfunction, and the hallmark symptom, post-exertional malaise. While the cause of this disease remains unknown, there is evidence of a potential infectious component [...] Read more.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disabling multisystem illness in which individuals are plagued with fatigue, inflammatory symptoms, cognitive dysfunction, and the hallmark symptom, post-exertional malaise. While the cause of this disease remains unknown, there is evidence of a potential infectious component that, along with patient symptoms and common onsets of the disease, implicates immune system dysfunction. To further our understanding of the state of ME/CFS lymphocytes, we characterized the role of fatty acids in isolated Natural Killer cells, CD4+ T cells, and CD8+ T cells in circulation and after overnight stimulation, through implicit perturbations to fatty acid oxidation. We examined samples obtained from at least 8 and as many as 20 subjects for immune cell fatty acid characterization in a variety of experiments and found that all three isolated cell types increased their utilization of lipids and levels of pertinent proteins involved in this metabolic pathway in ME/CFS samples, particularly during higher energy demands and activation. In T cells, we characterized the cell populations contributing to these metabolic shifts, which included CD4+ memory cells, CD4+ effector cells, CD8+ naïve cells, and CD8+ memory cells. We also discovered that patients with ME/CFS and healthy control samples had significant correlations between measurements of CD4+ T cell fatty acid metabolism and demographic data. These findings provide support for metabolic dysfunction in ME/CFS immune cells. We further hypothesize about the consequences that these altered fuel dependencies may have on T and NK cell effector function, which may shed light on the illness’s mechanism of action. Full article
(This article belongs to the Special Issue Metabolic Pathways in Immune Cells during Diseases)
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Review

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12 pages, 965 KiB  
Review
Immunometabolism of Immune Cells in Mucosal Environment Drives Effector Responses against Mycobacterium tuberculosis
by Mohd Hatimi Tukiman and Mohd Nor Norazmi
Int. J. Mol. Sci. 2022, 23(15), 8531; https://doi.org/10.3390/ijms23158531 - 1 Aug 2022
Cited by 6 | Viewed by 3533
Abstract
Tuberculosis remains a major threat to global public health, with more than 1.5 million deaths recorded in 2020. Improved interventions against tuberculosis are urgently needed, but there are still gaps in our knowledge of the host-pathogen interaction that need to be filled, especially [...] Read more.
Tuberculosis remains a major threat to global public health, with more than 1.5 million deaths recorded in 2020. Improved interventions against tuberculosis are urgently needed, but there are still gaps in our knowledge of the host-pathogen interaction that need to be filled, especially at the site of infection. With a long history of infection in humans, Mycobacterium tuberculosis (Mtb) has evolved to be able to exploit the microenvironment of the infection site to survive and grow. The immune cells are not only reliant on immune signalling to mount an effective response to Mtb invasion but can also be orchestrated by their metabolic state. Cellular metabolism was often overlooked in the past but growing evidence of its importance in the functions of immune cells suggests that it can no longer be ignored. This review aims to gain a better understanding of mucosal immunometabolism of resident effector cells, such as alveolar macrophages and mucosal-associated invariant T cells (MAIT cells), in response to Mtb infection and how Mtb manipulates them for its survival and growth, which could address our knowledge gaps while opening up new questions, and potentially be applied for future vaccination and therapeutic strategies. Full article
(This article belongs to the Special Issue Metabolic Pathways in Immune Cells during Diseases)
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13 pages, 958 KiB  
Review
Abnormal mTOR Activity in Pediatric Autoimmune Neuropsychiatric and MIA-Associated Autism Spectrum Disorders
by Ekaterina A. Trifonova, Zakhar S. Mustafin, Sergey A. Lashin and Alex V. Kochetov
Int. J. Mol. Sci. 2022, 23(2), 967; https://doi.org/10.3390/ijms23020967 - 16 Jan 2022
Cited by 4 | Viewed by 3906
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by the early onset of communication and behavioral problems. ASD is highly heritable; however, environmental factors also play a considerable role in this disorder. A significant part of both syndromic and idiopathic autism cases [...] Read more.
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by the early onset of communication and behavioral problems. ASD is highly heritable; however, environmental factors also play a considerable role in this disorder. A significant part of both syndromic and idiopathic autism cases could be attributed to disorders caused by mammalian target of rapamycin (mTOR)-dependent translation deregulation. This narrative review analyzes both bioinformatic and experimental evidence that connects mTOR signaling to the maternal autoantibody-related (MAR) autism spectrum and autoimmune neuropsychiatric disorders simultaneously. In addition, we reconstruct a network presenting the interactions between the mTOR signaling and eight MAR ASD genes coding for ASD-specific maternal autoantibody target proteins. The research discussed in this review demonstrates novel perspectives and validates the need for a subtyping of ASD on the grounds of pathogenic mechanisms. The utter necessity of designing ELISA-based test panels to identify all antibodies related to autism-like behavior is also considered. Full article
(This article belongs to the Special Issue Metabolic Pathways in Immune Cells during Diseases)
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