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Biomedicines
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The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases
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The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 11446

Special Issue Editors

Dr. Robert Gurke

E-Mail Website
Guest Editor
1. Fraunhofer Institute for Translational Medicine and Pharmacology (ITMP), and Fraunhofer Cluster of Excellence for Immune Mediated Diseases (CIMD), 60596 Frankfurt am Main, Germany
2. Institute of Clinical Pharmacology, Medical Faculty, Goethe-University Frankfurt, 60590 Frankfurt, Germany
Interests: lipidomics; LC-MS(/MS); biomedical analytics; pre-analytical sample handling; multiomics; biochemistry; immune-mediated diseases; biomarker; systems medicine
Dr. Marco Sisignano

E-Mail Website
Guest Editor
1. Fraunhofer Institute for Translational Medicine and Pharmacology (ITMP), and Fraunhofer Cluster of Excellence for Immune Mediated Diseases (CIMD), 60596 Frankfurt am Main, Germany
2. Institute of Clinical Pharmacology, Medical Faculty, Goethe-University Frankfurt, 60590 Frankfurt, Germany
Interests: biomedical research; neuro-immune interactions; pain; lipid signaling; personalized medicine; mass spectrometry based lipidomics; multiomics; pharmacology; biochemstry; cell biology; neurobiology; lipid-related GPCRs; TRP channels

Special Issue Information

Dear Colleagues,

Immune-mediated diseases (IMDs) are a widespread burden to human society. Around 10% of the global population suffer from an autoimmune or autoinflammatory disease, like systemic lupus erythematodes, plaque psoriasis, multiple sclerosis or rheumatoid arthritis. Chronic inflammation can also aggravate pain states and can lead to dysfunctional or neuropathic pain. Traditionally, IMDs are assessed by common clinical outcomes, suggesting comparable pathophysiological features and a similar response to therapeutic interventions. However, in reality, everyone differs in terms of their susceptibility to disease, the manner in which a disease occurs and progresses, the clinical phenotype that is displayed and the most appropriate drugs and dosing regimen to improve health and quality of life. Taken to its logical extreme, we need precision medicine in which every patient is considered unique, and a bespoke disease category and therapeutic strategy are assigned on a case-by-case basis. To achieve this objective, it is of utmost importance to gain a clearer understanding of the pathogenesis of IMDs. As lipid mediators and lipid signaling play a fundamental role in the immune system and changes thereof are closely related to IMDs, lipidomics analysis is a promising strategy to reach this goal. Therefore, it is the aim of this Special Issue to place a special focus on lipids as an essential part of the pathogenesis of IMDs.

Dr. Robert Gurke
Dr. Marco Sisignano
Guest Editors

Manuscript Submission Information

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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

  • lipidomics
  • biochemistry
  • immune-mediated diseases
  • inflammation
  • lipid signaling
  • lipid mediators
  • pathogenesis
  • lipid-related GPCRs and other receptors
  • pharmacology

Published Papers (5 papers)

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Research

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11 pages, 2299 KiB  
Article
Untargeted Lipidomics Reveals Characteristic Biomarkers in Patients with Ankylosing Spondylitis Disease
by Zhengjun Li, Wanjian Gu, Yingzhuo Wang, Bin Qin, Wei Ji, Zhongqiu Wang and Shijia Liu
Biomedicines 2023, 11(1), 47; https://doi.org/10.3390/biomedicines11010047 - 25 Dec 2022
Cited by 2 | Viewed by 1195
Abstract
Objective. Ankylosing spondylitis (AS) is a chronic inflammatory disease of the axial skeleton. Early and accurate diagnosis is necessary for the timely and effective treatment of this disease and its common complications. Lipid metabolites form various kinds of bioactive molecules that regulate the [...] Read more.
Objective. Ankylosing spondylitis (AS) is a chronic inflammatory disease of the axial skeleton. Early and accurate diagnosis is necessary for the timely and effective treatment of this disease and its common complications. Lipid metabolites form various kinds of bioactive molecules that regulate the initiation and progression of inflammation. However, there are currently few studies that investigate the alteration of serum lipid in AS patients. Methods. Blood samples were collected from 115 AS patients and 108 healthy controls (HCs). Serum-untargeted lipidomics were performed using ultrahigh-performance liquid chromatography coupled with Q-Exactive spectrometry, and the data were determined by multivariate statistical methods to explore potential lipid biomarkers. Results. Lipid phenotypes associated with disease activity were detected in the serum of patients with AS. Of all 586 identified lipids, there are 297 differential lipid metabolites between the AS and HC groups, of which 15 lipid metabolites are significant. In the AS groups, the levels of triacylglycerol (TAG) (18:0/18:1/20:0) were increased, and the levels of phosphatidylcholine (PC) (16:0e/26:4) and PC (18:1/22:6) were decreased. The areas under the receiver operating characteristic curve (AUC) of TAG (18:0/18:1/20:0), PC (16:0e/26:4), and PC (18:1/22:6) were 0.919, 0.843, and 0.907, respectively. Conclusion. Our findings uncovered that lipid deregulation is a crucial hallmark of AS, thereby providing new insights into the early diagnosis of AS. Full article
(This article belongs to the Special Issue The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases)
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12 pages, 1410 KiB  
Article
2-Arachidonoylglycerol Reduces the Production of Interferon-Gamma in T Lymphocytes from Patients with Systemic Lupus Erythematosus
by Luca Navarini, Marta Vomero, Stefano Di Donato, Damiano Currado, Onorina Berardicurti, Annalisa Marino, Pietro Bearzi, Alice Biaggi, Matteo Ferrito, Piero Ruscitti, Marina Fava, Alessandro Leuti, Paola Cipriani, Mauro Maccarrone and Roberto Giacomelli
Biomedicines 2022, 10(7), 1675; https://doi.org/10.3390/biomedicines10071675 - 12 Jul 2022
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Abstract
Background: the endocannabinoid 2-arachidonoylglycerol (2-AG) plays a pivotal role in immune cells regulation. The plasma levels of 2-AG are increased in patients with systemic lupus erythematosus (SLE) and correlate with disease activity. Moreover, in plasmacytoid dendritic cells from SLE patients, 2-AG is [...] Read more.
Background: the endocannabinoid 2-arachidonoylglycerol (2-AG) plays a pivotal role in immune cells regulation. The plasma levels of 2-AG are increased in patients with systemic lupus erythematosus (SLE) and correlate with disease activity. Moreover, in plasmacytoid dendritic cells from SLE patients, 2-AG is able to control the production of type 1 interferon (IFN) through CB2 activation. The aim of this study was to evaluate the potential role of 2-AG on T lymphocytes from SLE patients. Methods: peripheral blood mononuclear cells (PBMCs) from SLE participants and age- and sex-matched healthy donors (HD) were isolated by Ficoll–Hypaque density-gradient centrifugation. The PBMCs were treated with increasing concentrations of 2-AG, and AM251 and AM630 were used to antagonize CB1 and CB2, respectively. Flow cytometry was used to assess the expression of CD3, CD4, CD8, CD25, IFN-ɣ, IL-4, and IL-17A. Results: 2-AG (1 μM) decreased IFN-ɣ expression (p = 0.0005) in the Th1 lymphocytes of SLE patients. 2-AG did not modulate the cytokine expression of any other T lymphocyte population from either SLE or HD. Treatment with both 2-AG and AM630 increased the IFN-ɣ expression in Th1 lymphocytes of SLE patients (p = 0.03). Discussion: 2-AG is able to modulate type 2 IFN production from CD4+ T lymphocytes from SLE patients through CB2 activation. Full article
(This article belongs to the Special Issue The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases)
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22 pages, 2000 KiB  
Article
Male Knock-in Mice Expressing an Arachidonic Acid Lipoxygenase 15B (Alox15B) with Humanized Reaction Specificity Are Prematurely Growth Arrested When Aging
by Marjann Schäfer, Kumar R. Kakularam, Florian Reisch, Michael Rothe, Sabine Stehling, Dagmar Heydeck, Gerhard P. Püschel and Hartmut Kuhn
Biomedicines 2022, 10(6), 1379; https://doi.org/10.3390/biomedicines10061379 - 10 Jun 2022
Cited by 9 | Viewed by 1793
Abstract
Mammalian arachidonic acid lipoxygenases (ALOXs) have been implicated in cell differentiation and in the pathogenesis of inflammation. The mouse genome involves seven functional Alox genes and the encoded enzymes share a high degree of amino acid conservation with their human orthologs. There are, [...] Read more.
Mammalian arachidonic acid lipoxygenases (ALOXs) have been implicated in cell differentiation and in the pathogenesis of inflammation. The mouse genome involves seven functional Alox genes and the encoded enzymes share a high degree of amino acid conservation with their human orthologs. There are, however, functional differences between mouse and human ALOX orthologs. Human ALOX15B oxygenates arachidonic acid exclusively to its 15-hydroperoxy derivative (15S-HpETE), whereas 8S-HpETE is dominantly formed by mouse Alox15b. The structural basis for this functional difference has been explored and in vitro mutagenesis humanized the reaction specificity of the mouse enzyme. To explore whether this mutagenesis strategy may also humanize the reaction specificity of mouse Alox15b in vivo, we created Alox15b knock-in mice expressing the arachidonic acid 15-lipoxygenating Tyr603Asp+His604Val double mutant instead of the 8-lipoxygenating wildtype enzyme. These mice are fertile, display slightly modified plasma oxylipidomes and develop normally up to an age of 24 weeks. At later developmental stages, male Alox15b-KI mice gain significantly less body weight than outbred wildtype controls, but this effect was not observed for female individuals. To explore the possible reasons for the observed gender-specific growth arrest, we determined the basic hematological parameters and found that aged male Alox15b-KI mice exhibited significantly attenuated red blood cell parameters (erythrocyte counts, hematocrit, hemoglobin). Here again, these differences were not observed in female individuals. These data suggest that humanization of the reaction specificity of mouse Alox15b impairs the functionality of the hematopoietic system in males, which is paralleled by a premature growth arrest. Full article
(This article belongs to the Special Issue The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases)
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Review

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17 pages, 1682 KiB  
Review
Hepatitis C Virus-Lipid Interplay: Pathogenesis and Clinical Impact
by Wesal Elgretli, Tianyan Chen, Nadine Kronfli and Giada Sebastiani
Biomedicines 2023, 11(2), 271; https://doi.org/10.3390/biomedicines11020271 - 19 Jan 2023
Cited by 7 | Viewed by 4072
Abstract
Hepatitis C virus (HCV) infection represents the major cause of chronic liver disease, leading to a wide range of hepatic diseases, including cirrhosis and hepatocellular carcinoma. It is the leading indication for liver transplantation worldwide. In addition, there is a growing body of [...] Read more.
Hepatitis C virus (HCV) infection represents the major cause of chronic liver disease, leading to a wide range of hepatic diseases, including cirrhosis and hepatocellular carcinoma. It is the leading indication for liver transplantation worldwide. In addition, there is a growing body of evidence concerning the role of HCV in extrahepatic manifestations, including immune-related disorders and metabolic abnormalities, such as insulin resistance and steatosis. HCV depends on its host cells to propagate successfully, and every aspect of the HCV life cycle is closely related to human lipid metabolism. The virus circulates as a lipid-rich particle, entering the hepatocyte via lipoprotein cell receptors. It has also been shown to upregulate lipid biosynthesis and impair lipid degradation, resulting in significant intracellular lipid accumulation (steatosis) and circulating hypocholesterolemia. Patients with chronic HCV are at increased risk for hepatic steatosis, dyslipidemia, and cardiovascular disease, including accelerated atherosclerosis. This review aims to describe different aspects of the HCV viral life cycle as it impacts host lipoproteins and lipid metabolism. It then discusses the mechanisms of HCV-related hepatic steatosis, hypocholesterolemia, and accelerated atherosclerosis. Full article
(This article belongs to the Special Issue The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases)
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11 pages, 1039 KiB  
Review
Features of Lipid Metabolism Disorders in Primary Biliary Cholangitis
by Vasiliy I. Reshetnyak and Igor V. Maev
Biomedicines 2022, 10(12), 3046; https://doi.org/10.3390/biomedicines10123046 - 25 Nov 2022
Cited by 4 | Viewed by 2080
Abstract
Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune liver disease that mostly affects women. A progressive disorder in the processes of bile secretion and enterohepatic bile salts circulation in patients with PBC already in its early stages, leading [...] Read more.
Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune liver disease that mostly affects women. A progressive disorder in the processes of bile secretion and enterohepatic bile salts circulation in patients with PBC already in its early stages, leading to an insufficient release of bile acids into the bowel and their entry into the systemic circulation. Insufficient bile acids released into the duodenum contributes to the development of malabsorption, energy malnutrition, and slowly progressive weight loss. The pathophysiological mechanisms of weight loss and its slow progression are associated with the deterioration of the fat emulsification processes and with the reduced absorption of hydrolyzed products, such as fatty acids and monoglycerides, with steatorrhea in patients with PBC, as well as in those with gut dysbiosis. Just in the early stages of the disease, this results in accelerated fatty acid β-oxidation that is aimed at compensating for progressive energy malnutrition. The entry of bile acids into the systemic circulation in PBC is accompanied by dyslipidemia. The mechanism of hyperlipidemia in patients with PBC differs from that in other conditions because along with an increase in total cholesterol (TC), there are elevated high-density lipoprotein levels and the appearance of unusual lipoprotein X (Lp-X). The appearance of Lp-X is most likely to be the body’s protective reaction to inactivate the detergent effect of bile acids on the membrane structures of blood corpuscles and vascular endothelial cells. It is bile acids, rather than TC levels, that correlate with the content of Lp-X and determine its formation. Concomitant hypercholesterolemia in patients with PBC is also aimed at neutralizing the detergent effect of bile acids that have entered the systemic circulation and is most likely a compensatory reaction of the body. “Anomalous” hypercholesterolemia in PBC can serve as a model system for the search and development of new methods for the treatment of dyslipidemia since it occurs without an increase in the incidence of cardiovascular events. Full article
(This article belongs to the Special Issue The Role of Lipids in the Pathogenesis of Immune-Mediated Diseases)
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