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Molecular Mechanisms of Immune Cell Function in Obesity and Related...
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Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (20 February 2023) | Viewed by 24915

Special Issue Editor

Prof. Dr. Beiyan Zhou

E-Mail Website
Guest Editor
Department of Immunology, University of Connecticut, Farmington, CT, USA
Interests: obesity-induced health risks; cardiovascular diseases

Special Issue Information

Dear Colleagues,

Obesity is a well-recognized health risk for various diseases. Characterized with metabolic and immunologic abnormalities, obesity has been associated with a wide variety of chronic diseases including type 2 diabetes, cardiovascular diseases, and some cancers, as well as compromised acute response to pathogen invasion. It is a crucial task to understand how immune cells contribute to obesity-induced health risk, and more importantly, how such knowledge can be translated to prevention/intervention strategy to mitigate obesity-associated diseases. Recent discoveries on this topic have provided valuable information to understand the molecular mechanisms underlying immune cells actions under obesity stress at genetic, transcriptomic, and epigenetic levels. This Special Issue on “Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases” aims to provide a comprehensive overview of the most recent advances in this timely topic and a preview to future research directions and challenges to mitigate obesity-induced health risks.

Prof. Dr. Beiyan Zhou
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. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • obesity
  • obesity-associated inflammation
  • metabolic syndromes
  • cardiovascular diseases
  • transcriptomics
  • epigenetics

Published Papers (5 papers)

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Research

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12 pages, 1924 KiB  
Communication
Ablation of Ghrelin Receptor Mitigates the Metabolic Decline of Aging Skeletal Muscle
by Colleen O’Reilly, Ligen Lin, Hongying Wang, James Fluckey and Yuxiang Sun
Genes 2022, 13(8), 1368; https://doi.org/10.3390/genes13081368 - 30 Jul 2022
Cited by 1 | Viewed by 2124
Abstract
The orexigenic hormone ghrelin has multifaceted roles in health and disease. We have reported that ablation of the ghrelin receptor, growth hormone secretagogue receptor (GHS-R), protects against metabolic dysfunction of adipose tissues in aging. Our further observation interestingly revealed that GHS-R deficiency phenocopies [...] Read more.
The orexigenic hormone ghrelin has multifaceted roles in health and disease. We have reported that ablation of the ghrelin receptor, growth hormone secretagogue receptor (GHS-R), protects against metabolic dysfunction of adipose tissues in aging. Our further observation interestingly revealed that GHS-R deficiency phenocopies the effects of myokine irisin. In this study, we aim to determine whether GHS-R affects the metabolic functions of aging skeletal muscle and whether GHS-R regulates the muscular functions via irisin. We first studied the expression of metabolic signature genes in gastrocnemius muscle of young, middle-aged and old mice. Then, old GHS-R knockout (Ghsr−/−) mice and their wild type counterparts were used to assess the impact of GHS-R ablation on the metabolic characteristics of gastrocnemius and soleus muscle. There was an increase of GHS-R expression in skeletal muscle during aging, inversely correlated with the decline of metabolic functions. Remarkedly the muscle of old GHS-R knockout (Ghsr−/−) mice exhibited a youthful metabolic profile and better maintenance of oxidative type 2 muscle fibers. Furthermore, old Ghsr−/− mice showed improved treadmill performance, supporting better functionality. Also intriguing to note was the fact that old GHS-R-ablated mice showed increased expression of the irisin precursor FNDC5 in the muscle and elevated plasma irisin levels in circulation, which supports a potential interrelationship between GHS-R and irisin. Overall, our work suggests that GHS-R has deleterious effects on the metabolism of aging muscle, which may be at least partially mediated by myokine irisin. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases)
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Review

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12 pages, 660 KiB  
Review
Macrophages at the Crossroad of Meta-Inflammation and Inflammaging
by Lili Qu, Alyssa J. Matz, Keaton Karlinsey, Ziming Cao, Anthony T. Vella and Beiyan Zhou
Genes 2022, 13(11), 2074; https://doi.org/10.3390/genes13112074 - 9 Nov 2022
Cited by 11 | Viewed by 2288
Abstract
Macrophages are central players in systemic inflammation associated with obesity and aging, termed meta-inflammation and inflammaging. Activities of macrophages elicited by the two chronic conditions display shared and distinct patterns mechanistically, resulting in multifaceted actions for their pathogenic roles. Drastically expanded tissue macrophage [...] Read more.
Macrophages are central players in systemic inflammation associated with obesity and aging, termed meta-inflammation and inflammaging. Activities of macrophages elicited by the two chronic conditions display shared and distinct patterns mechanistically, resulting in multifaceted actions for their pathogenic roles. Drastically expanded tissue macrophage populations under obesity and aging stress attribute to both enhanced recruitment and local expansion. Importantly, molecular networks governing the multifaceted actions of macrophages are directly altered by environmental cues and subsequently contribute to metabolic reprogramming, resulting in meta-inflammation in obesity or inflammaging in aging. In this review, we will summarize how meta-inflammation and inflammaging affect macrophages and the molecular mechanisms involved in these processes. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases)
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Graphical abstract

16 pages, 626 KiB  
Review
Obesity and Adipose Tissue Dysfunction: From Pediatrics to Adults
by Ana Menendez, Heather Wanczyk, Joanne Walker, Beiyan Zhou, Melissa Santos and Christine Finck
Genes 2022, 13(10), 1866; https://doi.org/10.3390/genes13101866 - 15 Oct 2022
Cited by 10 | Viewed by 4558
Abstract
Obesity is a growing health problem that affects both children and adults. The increasing prevalence of childhood obesity is associated with comorbidities such as cardiovascular disease, type 2 diabetes and metabolic syndrome due to chronic low-grade inflammation present at early stages of the [...] Read more.
Obesity is a growing health problem that affects both children and adults. The increasing prevalence of childhood obesity is associated with comorbidities such as cardiovascular disease, type 2 diabetes and metabolic syndrome due to chronic low-grade inflammation present at early stages of the disease. In pediatric patients suffering from obesity, the role of epigenetics, the gut microbiome and intrauterine environment have emerged as causative factors Interestingly, pediatric obesity is strongly associated with low birth weight. Accelerated weight gain oftentimes occurs in these individuals during the post-natal period, which can lead to increased risk of adiposity and metabolic disease. The pathophysiology of obesity is complex and involves biological and physiological factors compounded by societal factors such as family and community. On a cellular level, adipocytes contained within adipose tissue become dysregulated and further contribute to development of comorbidities similar to those present in adults with obesity. This review provides an overview of the current understanding of adipose tissue immune, inflammatory and metabolic adaptation of the adipose tissue in obesity. Early cellular changes as well as the role of immune cells and inflammation on the progression of disease in pivotal pediatric clinical trials, adult studies and mouse models are emphasized. Understanding the initial molecular and cellular changes that occur during obesity can facilitate new and improved treatments aimed at early intervention and subsequent prevention of adulthood comorbidities. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases)
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27 pages, 990 KiB  
Review
Interleukin-17 Family Cytokines in Metabolic Disorders and Cancer
by Eileen Victoria Meehan and Kepeng Wang
Genes 2022, 13(9), 1643; https://doi.org/10.3390/genes13091643 - 13 Sep 2022
Cited by 16 | Viewed by 6304
Abstract
Interleukin-17 (IL-17) family cytokines are potent drivers of inflammatory responses. Although IL-17 was originally identified as a cytokine that induces protective effects against bacterial and fungal infections, IL-17 can also promote chronic inflammation in a number of autoimmune diseases. Research in the last [...] Read more.
Interleukin-17 (IL-17) family cytokines are potent drivers of inflammatory responses. Although IL-17 was originally identified as a cytokine that induces protective effects against bacterial and fungal infections, IL-17 can also promote chronic inflammation in a number of autoimmune diseases. Research in the last decade has also elucidated critical roles of IL-17 during cancer development and treatment. Intriguingly, IL-17 seems to play a role in the risk of cancers that are associated with metabolic disorders. In this review, we summarize our current knowledge on the biochemical basis of IL-17 signaling, IL-17′s involvement in cancers and metabolic disorders, and postulate how IL-17 family cytokines may serve as a bridge between these two types of diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases)
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10 pages, 1508 KiB  
Review
Macrophage Polarization in Atherosclerosis
by Sahar Eshghjoo, Da Mi Kim, Arul Jayaraman, Yuxiang Sun and Robert C. Alaniz
Genes 2022, 13(5), 756; https://doi.org/10.3390/genes13050756 - 25 Apr 2022
Cited by 37 | Viewed by 8924
Abstract
The implication of the heterogeneous spectrum of pro- and anti-inflammatory macrophages (Macs) has been an important area of investigation over the last decade. The polarization of Macs alters their functional phenotype in response to their surrounding microenvironment. Macs are the major immune cells [...] Read more.
The implication of the heterogeneous spectrum of pro- and anti-inflammatory macrophages (Macs) has been an important area of investigation over the last decade. The polarization of Macs alters their functional phenotype in response to their surrounding microenvironment. Macs are the major immune cells implicated in the pathogenesis of atherosclerosis. A hallmark pathology of atherosclerosis is the accumulation of pro-inflammatory M1-like macrophages in coronary arteries induced by pro-atherogenic stimuli; these M1-like pro-inflammatory macrophages are incapable of digesting lipids, thus resulting in foam cell formation in the atherosclerotic plaques. Recent findings suggest that the progression and stability of atherosclerotic plaques are dependent on the quantity of infiltrated Macs, the polarization state of the Macs, and the ratios of different types of Mac populations. The polarization of Macs is defined by signature markers on the cell surface, as well as by factors in intracellular and intranuclear compartments. At the same time, pro- and anti-inflammatory polarized Macs also exhibit different gene expression patterns, with differential cellular characteristics in oxidative phosphorylation and glycolysis. Macs are reflective of different metabolic states and various types of diseases. In this review, we discuss the major differences between M1-like Macs and M2-like Macs, their associated metabolic pathways, and their roles in atherosclerosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Immune Cell Function in Obesity and Related Diseases)
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