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Proteomics for the Study of Inflammatory Diseases

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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 (31 July 2023) | Viewed by 25851

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Special Issue Editors

Dr. Juan Antonio Fafián Labora

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Guest Editor

Cell Therapy and Regenerative Medicine Group, Department of Physiotherapy, Medicine and Biomedical Sciences, Faculty of Health Sciences, University of A Coruña (UDC), 15008 A Coruna, Spain
Interests: inflamm-ageing; ageing; protemics; small extracellular vesicles; cellular senescence; SASP; age-related diseases

Dr. Jesús Mateos

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Guest Editor

1. Santiago de Compostela Health Research Institute (IDIS), Complejo Hospitalario Universitario de Santiago de Compostela (CHUS), Santiago, Spain
2. Galápagos NV, 2800 Mechelen, Belgium
Interests: proteomics; tuberculosis; inflammatory diseases; aging; high throughput analysis; phosphoproteomics

Special Issue Information

Dear Colleagues,

Inflammation is a generic protective response of the body tissues against harmful agents of different origins. It is considered an innate immune response mechanism and characterized by heat, pain, redness, swelling, and loss of function. Inflammation has been classically classified as either acute or chronic, involving the action of different types of immune cells.

Both acute and chronic inflammatory processes are present in a plethora of disorders, such as cancer, atherosclerosis, obesity, allergy or bacterial/viral infections. Furthermore, in the last decade, inflammation has been revealed as key process in organism aging, thus introducing the concept of “inflammaging”. Age-associated accumulation of damage-associated molecular patterns (DAMPs) is an important trigger in inflammation and has been proposed as driver of inflammaging.

The recent technical advances in Liquid Chromatography coupled to Mass Spectrometry (LC-MS) and data processing allow not only a deeper understanding of the molecular processes specifically modulated in each disease, but also patient-based research for personalized medicine. In this Special Issue, we will present cutting edge advances in the use of proteomics tools for the study of the inflammatory diseases and treatment.

This Special Issue is about molecular science. Thus, pure clinical studies will not be suitable, but clinical submissions with biomolecular experiments are welcomed.

Dr. Juan Antonio Fafián Labora
Dr. Jesús Mateos
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

proteomics
mass spectrometry
chromatography
inflammatory diseases
immune response
allergy
infection
cancer
inflammaging
biomarker discovery
biological fluids
atherosclerosis
fibrosis
macrophages
extracellular vesicles

Published Papers (7 papers)

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Research

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21 pages, 4514 KiB

Open AccessArticle

Changes in Serum Protein–Peptide Patterns in Atopic Children Allergic to Plant Storage Proteins

by Kacper Packi, Joanna Matysiak, Eliza Matuszewska, Anna Bręborowicz and Jan Matysiak

Int. J. Mol. Sci. 2023, 24(2), 1804; https://doi.org/10.3390/ijms24021804 - 16 Jan 2023

Cited by 3 | Viewed by 2092

Abstract

Next to cow’s milk and eggs, plant foods, i.e., legumes, tree nuts and cereal grains, most often sensitise atopic children. Storage proteins constitutes the most relevant protein fraction of plant foods, causing primary sensitisation. They exhibit strong allergenic properties and immunogenicity. Our goal was to analyse sensitisation to 26 plant storage proteins in a group of 76 children aged 0–5 years with chronic symptoms of atopic dermatitis using Allergy Explorer ALEX2 and to discover changes in serum protein–peptide patterns in allergic patients with the use of MALDI-TOF-MS. We reported that 25% of children were allergic to 2S albumins, 19.7% to 7S globulins, 13.2% to 11S globulins and 1.3% to cereal prolamins. The most common allergenic molecules were Ara h 1 (18.4%), Ara h 2 (17.1%), Ara h 6 (15.8%) and Ara h 3 (11.8%) from peanuts, and the mean serum sIgE concentrations in allergic patients were 10.93 kUA/L, 15.353 kUA/L, 15.359 kUA/L and 9.038 kUA/L, respectively. In children allergic to storage proteins compared to the other patients (both allergic and non-allergic), the cell cycle control protein 50A, testis-expressed sequence 13B, DENN domain-containing protein 5A and SKI family transcriptional corepressor 2 were altered. Our results indicate that the IgE-mediated allergy to storage proteins is a huge problem in a group of young, atopic children, and show the potential of proteomic analysis in the prediction of primary sensitisation to plant foods. It is the next crucial step for understanding the molecular consequences of allergy to storage proteins. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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24 pages, 3334 KiB

Open AccessArticle

Multi-Omics Analysis Revealed a Significant Alteration of Critical Metabolic Pathways Due to Sorafenib-Resistance in Hep3B Cell Lines

by Kholoud Y. I. Abushawish, Sameh S. M. Soliman, Alexander D. Giddey, Hamza M. Al-Hroub, Muath Mousa, Karem H. Alzoubi, Waseem El-Huneidi, Eman Abu-Gharbieh, Hany A. Omar, Sara M. Elgendy, Yasser Bustanji, Nelson C. Soares and Mohammad H. Semreen

Int. J. Mol. Sci. 2022, 23(19), 11975; https://doi.org/10.3390/ijms231911975 - 9 Oct 2022

Cited by 6 | Viewed by 2591

Abstract

Hepatocellular carcinoma (HCC) is the second prominent cause of cancer-associated death worldwide. Usually, HCC is diagnosed in advanced stages, wherein sorafenib, a multiple target tyrosine kinase inhibitor, is used as the first line of treatment. Unfortunately, resistance to sorafenib is usually encountered within six months of treatment. Therefore, there is a critical need to identify the underlying reasons for drug resistance. In the present study, we investigated the proteomic and metabolomics alterations accompanying sorafenib resistance in hepatocellular carcinoma Hep3B cells by employing ultra-high-performance liquid chromatography quadrupole time of flight mass spectrometry (UHPLC-QTOF-MS). The Bruker Human Metabolome Database (HMDB) library was used to identify the differentially abundant metabolites through MetaboScape 4.0 software (Bruker). For protein annotation and identification, the Uniprot proteome for Homo sapiens (Human) database was utilized through MaxQuant. The results revealed that 27 metabolites and 18 proteins were significantly dysregulated due to sorafenib resistance in Hep3B cells compared to the parental phenotype. D-alanine, L-proline, o-tyrosine, succinic acid and phosphatidylcholine (PC, 16:0/16:0) were among the significantly altered metabolites. Ubiquitin carboxyl-terminal hydrolase isozyme L1, mitochondrial superoxide dismutase, UDP-glucose-6-dehydrogenase, sorbitol dehydrogenase and calpain small subunit 1 were among the significantly altered proteins. The findings revealed that resistant Hep3B cells demonstrated significant alterations in amino acid and nucleotide metabolic pathways, energy production pathways and other pathways related to cancer aggressiveness, such as migration, proliferation and drug-resistance. Joint pathway enrichment analysis unveiled unique pathways, including the antifolate resistance pathway and other important pathways that maintain cancer cells’ survival, growth, and proliferation. Collectively, the results identified potential biomarkers for sorafenib-resistant HCC and gave insights into their role in chemotherapeutic drug resistance, cancer initiation, progression and aggressiveness, which may contribute to better prognosis and chemotherapeutic outcomes. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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16 pages, 3401 KiB

Open AccessArticle

Cardiac Alarmins as Residual Risk Markers of Atherosclerosis under Hypolipidemic Therapy

by Viorel I. Suica, Elena Uyy, Luminita Ivan, Raluca M. Boteanu, Aurel Cerveanu-Hogas, Rune Hansen and Felicia Antohe

Int. J. Mol. Sci. 2022, 23(19), 11174; https://doi.org/10.3390/ijms231911174 - 22 Sep 2022

Viewed by 1573

Abstract

Increased levels of low-density lipoproteins are the main risk factor in the initiation and progression of atherosclerosis. Although statin treatment can effectively lower these levels, there is still a residual risk of cardiovascular events. We hypothesize that a specific panel of stress-sensing molecules (alarmins) could indicate the persistence of silent atherosclerosis residual risk. New Zealand White rabbits were divided into: control group (C), a group that received a high-fat diet for twelve weeks (Au), and a treated hyperlipidemic group with a lipid diet for eight weeks followed by a standard diet and hypolipidemic treatment (atorvastatin and PCSK9 siRNA-inhibitor) for four weeks (Asi). Mass spectrometry experiments of left ventricle lysates were complemented by immunologic and genomic studies to corroborate the data. The hyperlipidemic diet determined a general alarmin up-regulation tendency over the C group. A significant spectral abundance increase was measured for specific heat shock proteins, S100 family members, HMGB1, and Annexin A1. The hypolipidemic treatment demonstrated a reversed regulation trend with non-significant spectral alteration over the C group for some of the identified alarmins. Our study highlights the discriminating potential of alarmins in hyperlipidemia or following hypolipidemic treatment. Data are available via ProteomeXchange with identifier PXD035692. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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12 pages, 1903 KiB

Open AccessArticle

Histone Extraction from Human Articular Cartilage for the Study of Epigenetic Regulation in Osteoarthritis

by Carmen Núñez-Carro, Margarita Blanco-Blanco, Tatiana Montoya, Karla M. Villagrán-Andrade, Tamara Hermida-Gómez, Francisco J. Blanco and María C. de Andrés

Int. J. Mol. Sci. 2022, 23(6), 3355; https://doi.org/10.3390/ijms23063355 - 20 Mar 2022

Cited by 6 | Viewed by 2443

Abstract

Osteoarthritis (OA) is a chronic disease that affects articular cartilage, causing its degeneration. Although OA is one of the most prevalent pathologies globally, there are no definitive treatments available. Recently, research has focused on elucidating the complex interplay that takes place between inflammatory processes and epigenetic regulation, showing that histone post-translational modifications (PTMs) can exert a pronounced effect on the expression of OA-related genes. OA chondrocytes enhance the production of interleukin 1β (IL-1β) and interleukin 8 (IL-8), which are epigenetically regulated. These cytokines upregulate the synthesis of matrix metalloproteinases (MMPs) and aggrecanases, which promote the extracellular matrix (ECM) destruction. This motivates the study of histone PTMs to investigate the epigenetic regulation of proinflammatory molecules, but the absence of specific protocols to extract histones from human articular cartilage has complicated this task. The lack of effective methods can be explained by the structural complexity and low cellularity of this tissue, which are responsible for the biomechanical properties that allow the movement of the joint but also complicate histone isolation. Here, we provide a histone extraction procedure specifically adapted for cryopreserved human articular cartilage that can be useful to understand epigenetic regulation in OA and accelerate the search for novel strategies. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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18 pages, 3446 KiB

Open AccessArticle

New Proteins Contributing to Immune Cell Infiltration and Pannus Formation of Synovial Membrane from Arthritis Diseases

by Dominique de Seny, Dominique Baiwir, Elettra Bianchi, Gaël Cobraiville, Céline Deroyer, Christophe Poulet, Olivier Malaise, Geneviève Paulissen, Marie-Joëlle Kaiser, Jean-Philippe Hauzeur, Gabriel Mazzucchelli, Philippe Delvenne and Michel Malaise

Int. J. Mol. Sci. 2022, 23(1), 434; https://doi.org/10.3390/ijms23010434 - 31 Dec 2021

Cited by 7 | Viewed by 2401

Abstract

An inflamed synovial membrane plays a major role in joint destruction and is characterized by immune cells infiltration and fibroblast proliferation. This proteomic study considers the inflammatory process at the molecular level by analyzing synovial biopsies presenting a histological inflammatory continuum throughout different arthritis joint diseases. Knee synovial biopsies were obtained from osteoarthritis (OA; n = 9), chronic pyrophosphate arthropathy (CPPA; n = 7) or rheumatoid arthritis (RA; n = 8) patients. The histological inflammatory score was determined using a semi-quantitative scale based on synovial hyperplasia, lymphocytes, plasmocytes, neutrophils and macrophages infiltration. Proteomic analysis was performed by liquid chromatography-mass spectrometry (LC-MS/MS). Differentially expressed proteins were confirmed by immunohistochemistry. Out of the 1871 proteins identified and quantified by LC-MS/MS, 10 proteins (LAP3, MANF, LCP1, CTSZ, PTPRC, DNAJB11, EML4, SCARA5, EIF3K, C1orf123) were differentially expressed in the synovial membrane of at least one of the three disease groups (RA, OA and CPPA). Significant increased expression of the seven first proteins was detected in RA and correlated to the histological inflammatory score. Proteomics is therefore a powerful tool that provides a molecular pattern to the classical histology usually applied for synovitis characterization. Except for LCP1, CTSZ and PTPRC, all proteins have never been described in human synovitis. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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Review

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14 pages, 1139 KiB

Open AccessReview

Deciphering the Relationship between SARS-CoV-2 and Cancer

by Michele Costanzo, Maria Anna Rachele De Giglio and Giovanni Nicola Roviello

Int. J. Mol. Sci. 2023, 24(9), 7803; https://doi.org/10.3390/ijms24097803 - 25 Apr 2023

Cited by 9 | Viewed by 11070

Abstract

Some viruses are known to be associated with the onset of specific cancers. These microorganisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer cells by modulating the central metabolic pathways or hampering genomic integrity mechanisms, consequently inhibiting the apoptotic machinery and/or enhancing cell proliferation. Seven oncogenic viruses are known to promote tumorigenesis in humans: human papillomavirus (HPV), hepatitis B and C viruses (HBV, HCV), Epstein-Barr virus (EBV), human T-cell leukemia virus 1 (HTLV-1), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV). Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development. This hypothesis is based on the growing evidence regarding the ability of SARS-CoV-2 to modulate oncogenic pathways, promoting chronic low-grade inflammation and causing tissue damage. Herein, we summarize the main relationships known to date between virus infection and cancer, providing a summary of the proposed biochemical mechanisms behind the cellular transformation. Mechanistically, DNA viruses (such as HPV, HBV, EBV, and MCPyV) encode their virus oncogenes. In contrast, RNA viruses (like HCV, HTLV-1) may encode oncogenes or trigger host oncogenes through cis-/-trans activation leading to different types of cancer. As for SARS-CoV-2, its role as an oncogenic virus seems to occur through the inhibition of oncosuppressors or controlling the metabolic and autophagy pathways in the infected cells. However, these effects could be significant in particular scenarios like those linked to severe COVID-19 or long COVID. On the other hand, looking at the SARS-CoV-2─cancer relationship from an opposite perspective, oncolytic effects and anti-tumor immune response were triggered by SARS-CoV-2 infection in some cases. In summary, our work aims to recall comprehensive attention from the scientific community to elucidate the effects of SARS-CoV-2 and, more in general, β-coronavirus infection on cancer susceptibility for cancer prevention or supporting therapeutic approaches. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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22 pages, 8894 KiB

Open AccessReview

Recent Advances in Proteomics-Based Approaches to Studying Age-Related Macular Degeneration: A Systematic Review

by Laura García-Quintanilla, Lorena Rodríguez-Martínez, Enrique Bandín-Vilar, María Gil-Martínez, Miguel González-Barcia, Cristina Mondelo-García, Anxo Fernández-Ferreiro and Jesús Mateos

Int. J. Mol. Sci. 2022, 23(23), 14759; https://doi.org/10.3390/ijms232314759 - 25 Nov 2022

Cited by 5 | Viewed by 2481

Abstract

Age-related macular degeneration (AMD) is a common ocular disease characterized by degeneration of the central area of the retina in the elderly population. Progression and response to treatment are influenced by genetic and non-genetic factors. Proteomics is a powerful tool to study, at the molecular level, the mechanisms underlying the progression of the disease, to identify new therapeutic targets and to establish biomarkers to monitor progression and treatment effectiveness. In this work, we systematically review the use of proteomics-based approaches for the study of the molecular mechanisms underlying the development of AMD, as well as the progression of the disease and on-treatment patient monitoring. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) reporting guidelines were followed. Proteomic approaches have identified key players in the onset of the disease, such as complement components and proteins involved in lipid metabolism and oxidative stress, but also in the progression to advanced stages, including factors related to extracellular matrix integrity and angiogenesis. Although anti-vascular endothelial growth factor (anti-VEGF)-based therapy has been crucial in the treatment of neovascular AMD, it is necessary to deepen our understanding of the underlying disease mechanisms to move forward to next-generation therapies for later-stage forms of this multifactorial disease. Full article

(This article belongs to the Special Issue Proteomics for the Study of Inflammatory Diseases)

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