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New Molecular Mechanisms and Markers in Inflammatory Disorders, 2nd Edition

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Dear Colleagues,

Inflammation participates in hosts’ defences against infectious agents and injury, but it also contributes to the pathophysiology of many chronic diseases, ranging from cancer to biomechanical injuries and from chronic to acute disorders. For this reason, the discovery of new, inflammation-linked biomarkers is the goal of many studies focused on the pathogenesis, the diagnosis, the prognosis, and the therapeutical approaches of inflammation-associated comorbidities. The intent of this Special Issue is to present research papers and reviews focused on new biomarkers of inflammation-associated disorders, which highlight their molecular mechanisms during the onset and progression of pathological states such as cancer, immune diseases, cardiovascular-associated disorders, metabolic diseases, and all other pathological states linked to inflammation. This knowledge should facilitate the development of novel strategies to predict disease susceptibility, target and monitor therapies, and ultimately, develop new approaches to the prevention and treatment of diseases associated with inflammation.

Dr. Galliera Emanuela Rita
Dr. Elena Vianello
Guest Editors

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Keywords

inflammation
inflammatory disorders
biomarkers
molecular mechanism of inflammation
molecular signaling

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Research

20 pages, 3749 KiB

Open AccessArticle

Serological Antibodies against Kidney, Liver, and Spleen Membrane Antigens as Potential Biomarkers in Patients with Immune Disorders

by Leidi Hernandez-Suarez, Eguzkiñe Diez-Martin, June Egiguren-Ortiz, Roberto Fernandez, Aitor Etxebarria, Egoitz Astigarraga, Cristina Miguelez, Andoni Ramirez-Garcia and Gabriel Barreda-Gómez

Int. J. Mol. Sci. 2024, 25(4), 2025; https://doi.org/10.3390/ijms25042025 - 07 Feb 2024

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Abstract

Immune disorders arise from complex genetic and environmental factors, which lead to dysregulation at the cellular and inflammatory levels and cause tissue damage. Recent research highlights the crucial role of reactive antibodies in autoimmune diseases and graft rejection, but their complex determination poses challenges for clinical use. Therefore, our study aimed to ascertain whether the presence of reactive antibodies against membrane antigens in tissues from both animal models and humans could serve as biomarkers in patients with autoimmune disorders. To address this issue, we examined the binding profile of serological antibodies against a diverse panel of cell membranes from the spleen, liver, and kidney tissues of monkeys, rats, and humans. After developing the cell membrane microarrays, human sera were immunologically assayed. The study was first conducted on sera from two groups, healthy subjects and patients with inflammatory and autoimmune disorders, and then optimized for kidney transplant patient sera. A significant increase in antibody reactivity against specific monkey kidney and spleen membranes was observed in the serum of patients with lupus nephritis, while kidney transplant patients showed a significant enhancement against human tissues and human embryonic kidney 293 cells. These results show the potential importance for clinical and basic research purposes of studying the presence of specific IgG against membrane antigens in patients’ serum as potential biomarkers of immune disorders. However, it is important to note that these results need to be verified in further studies with a larger sample size to confirm their relevance. Full article

(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 2nd Edition)

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16 pages, 1479 KiB

Open AccessArticle

Patterns of IgA Autoantibody Generation, Inflammatory Responses and Extracellular Matrix Metabolism in Patients with Alcohol Use Disorder

by Onni Niemelä, Aini Bloigu, Risto Bloigu, Ulla Nivukoski, Johanna Kultti and Heidi Pohjasniemi

Int. J. Mol. Sci. 2023, 24(17), 13124; https://doi.org/10.3390/ijms241713124 - 23 Aug 2023

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Abstract

Recent data have emphasized the role of inflammation and intestinal immunoglobulin A (IgA) responses in the pathogenesis of alcoholic liver disease (ALD). In order to further explore such associations, we compared IgA titers against antigens targeted to ethanol metabolites and tissue transglutaminase with pro- and anti-inflammatory mediators of inflammation, markers of liver status, transferrin protein desialylation and extracellular matrix metabolism in alcohol-dependent patients with or without liver disease and in healthy controls. Serum IgAs against protein adducts with acetaldehyde (HbAch-IgA), the first metabolite of ethanol, and tissue transglutaminase (tTG-IgA), desialylated transferrin (CDT), pro- and anti-inflammatory cytokines, markers of liver status (GT, ALP) and extracellular matrix metabolism (PIIINP, PINP, hyaluronic acid, ICTP and CTx) were measured in alcohol-dependent patients with (n = 83) or without (n = 105) liver disease and 88 healthy controls representing either moderate drinkers or abstainers. In ALD patients, both tTG-IgA and HbAch-IgA titers were significantly higher than those in the alcoholics without liver disease (p < 0.0005 for tTG-IgA, p = 0.006 for Hb-Ach-IgA) or in healthy controls (p < 0.0005 for both comparisons). The HbAch-IgA levels in the alcoholics without liver disease also exceeded those found in healthy controls (p = 0.0008). In ROC analyses, anti-tTG-antibodies showed an excellent discriminative value in differentiating between ALD patients and healthy controls (AUC = 0.95, p < 0.0005). Significant correlations emerged between tTG-IgAs and HbAch-IgAs (r_s = 0.462, p < 0.0005), CDT (r_s = 0.413, p < 0.0001), GT (r_s = 0.487, p < 0.0001), alkaline phosphatase (r_s = 0.466, p < 0.0001), serum markers of fibrogenesis: PIIINP (r_s = 0.634, p < 0.0001), hyaluronic acid (r_s = 0.575, p < 0.0001), ICTP (r_s = 0.482, p < 0.0001), pro-inflammatory cytokines IL-6 (r_s = 0.581, p < 0.0001), IL-8 (r_s = 0.535, p < 0.0001) and TNF-α (r_s = 0.591, p < 0.0001), whereas significant inverse correlations were observed with serum TGF-β (r_s = −0.366, p < 0.0001) and CTx, a marker of collagen degradation (r_s = −0.495, p < 0.0001). The data indicate that the induction of IgA immune responses toward ethanol metabolites and tissue transglutaminaseis a characteristic feature of patients with AUD and coincides with the activation of inflammation, extracellular matrix remodeling and the generation of aberrantly glycosylated proteins. These processes appear to work in concert in the sequence of events leading from heavy drinking to ALD. Full article

(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 2nd Edition)

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