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Exploring Molecular Mechanisms of Inflammatory Diseases
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Exploring Molecular Mechanisms of Inflammatory Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 6534

Special Issue Editor

Dr. Vlatka Sotosek

E-Mail Website
Guest Editor
1. Department of Anesthesiology, Reanimatology, Emergency and Intensive Medicine, Faculty of Medicine, University of Rijeka, 51 000 Rijeka, Croatia
2. Department of Clinical Medical Science II, Faculty od Health Studies, University of Rijeka, 51 000 Rijeka, Croatia
Interests: anesthesia; intensive medicine; immunity

Special Issue Information

Dear Colleagues,

We would like to invite you to submit your valuable manuscript for the upcoming issue of International Journal of Molecular Sciences, Impact Factor 6.208.

Journal is organizing a special issue on “Exploring Molecular Mechanisms of Inflammatory Diseases”. Inflammation is a protective response to noxious stimuli that unavoidably occurs at a cost to normal tissue function. Inflammatory diseases include a vast range of conditions and disorders. Different alternatives of pharmaceutical formulations have been used for the treatment where inflammation has its main role, as well as drug delivery systems, including liposomes, nanoparticles (lipid and polymeric), nanocrystals, dendrimers, niosomes, and micelles.

This Special Issue of IJMS will focus on the molecular and cellular advances in the pathogenesis and treatment of Inflammatory Diseases. The journal is now inviting submissions of research work and reviews for the possible publication in current edition. We would be glad if you can consider our request.

Dr. Vlatka Sotosek
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. 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

  • immunity
  • inflammation
  • inflammatory disease

Published Papers (3 papers)

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Research

23 pages, 2689 KiB  
Article
CXCL13 in Cerebrospinal Fluid: Clinical Value in a Large Cross-Sectional Study
by Deborah Katharina Erhart, Veronika Klose, Tatjana Schäper, Hayrettin Tumani and Makbule Senel
Int. J. Mol. Sci. 2024, 25(1), 425; https://doi.org/10.3390/ijms25010425 - 28 Dec 2023
Cited by 2 | Viewed by 820
Abstract
C-X-C-motif chemokine ligand 13 (CXCL13) in cerebrospinal fluid (CSF) is increasingly used in clinical routines, although its diagnostic specificity and divergent cut-off values have been defined so far mainly for neuroborreliosis. Our aim was to evaluate the value of CSF-CXCL13 as a diagnostic [...] Read more.
C-X-C-motif chemokine ligand 13 (CXCL13) in cerebrospinal fluid (CSF) is increasingly used in clinical routines, although its diagnostic specificity and divergent cut-off values have been defined so far mainly for neuroborreliosis. Our aim was to evaluate the value of CSF-CXCL13 as a diagnostic and treatment response marker and its role as an activity marker in a larger disease spectrum, including neuroborreliosis and other neuroinflammatory and malignant CNS-disorders. Patients who received a diagnostic lumbar puncture (LP) (n = 1234) between July 2009 and January 2023 were included in our retrospective cross-sectional study. The diagnostic performance of CSF-CXCL13 for acute neuroborreliosis was highest at a cut-off of 428.92 pg/mL (sensitivity: 92.1%; specificity: 96.5%). In addition, CXCL13 levels in CSF were significantly elevated in multiple sclerosis with clinical (p = 0.001) and radiographic disease activity (p < 0.001). The clinical utility of CSF-CXCL13 appears to be multifaceted. CSF-CXCL13 is significantly elevated in patients with neuroborreliosis and shows a rapid and sharp decline with antibiotic therapy, but it is not specific for this disease and is also highly elevated in less common subacute neuroinfectious diseases, such as neurosyphilis and cryptococcal meningitis or in primary/secondary B-cell lymphoma. Full article
(This article belongs to the Special Issue Exploring Molecular Mechanisms of Inflammatory Diseases)
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21 pages, 3997 KiB  
Article
Investigating Antibody Reactivity to the Intestinal Microbiome in Severe Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Feasibility Study
by Katharine A. Seton, Marianne Defernez, Andrea Telatin, Sumeet K. Tiwari, George M. Savva, Antonietta Hayhoe, Alistair Noble, Ana L. S. de Carvalho-KoK, Steve A. James, Amolak Bansal, Thomas Wileman and Simon R. Carding
Int. J. Mol. Sci. 2023, 24(20), 15316; https://doi.org/10.3390/ijms242015316 - 18 Oct 2023
Viewed by 4016
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multisystemic disease of unknown aetiology that is characterised by disabling chronic fatigue and involves both the immune and gastrointestinal (GI) systems. Patients display alterations in GI microbiome with a significant proportion experiencing GI discomfort and pain [...] Read more.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multisystemic disease of unknown aetiology that is characterised by disabling chronic fatigue and involves both the immune and gastrointestinal (GI) systems. Patients display alterations in GI microbiome with a significant proportion experiencing GI discomfort and pain and elevated blood biomarkers for altered intestinal permeability compared with healthy individuals. To investigate a possible GI origin of ME/CFS we designed a feasibility study to test the hypothesis that ME/CFS pathogenesis is a consequence of increased intestinal permeability that results in microbial translocation and a breakdown in immune tolerance leading to generation of antibodies reactive to indigenous intestinal microbes. Secretory immunoglobulin (Ig) A and serum IgG levels and reactivity to intestinal microbes were assessed in five pairs of severe ME/CFS patients and matched same-household healthy controls. For profiling serum IgG, we developed IgG-Seq which combines flow-cytometry based bacterial cell sorting and metagenomics to detect mucosal IgG reactivity to the microbiome. We uncovered evidence for immune dysfunction in severe ME/CFS patients that was characterised by reduced capacity and reactivity of serum IgG to stool microbes, irrespective of their source. This study provides the rationale for additional studies in larger cohorts of ME/CFS patients to further explore immune–microbiome interactions. Full article
(This article belongs to the Special Issue Exploring Molecular Mechanisms of Inflammatory Diseases)
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23 pages, 5588 KiB  
Article
Investigating the Molecular Mechanisms Underlying Early Response to Inflammation and Helicobacter pylori Infection in Human Gastric Epithelial Cells
by Giulia Martinelli, Marco Fumagalli, Stefano Piazza, Nicole Maranta, Francesca Genova, Paola Sperandeo, Enrico Sangiovanni, Alessandra Polissi, Mario Dell’Agli and Emma De Fabiani
Int. J. Mol. Sci. 2023, 24(20), 15147; https://doi.org/10.3390/ijms242015147 - 13 Oct 2023
Cited by 1 | Viewed by 1143
Abstract
Helicobacter pylori is a leading cause of chronic gastric inflammation, generally associated with gastritis and adenocarcinoma. Activation of the NF-κB pathway mainly contributes to the inflammatory phenotype observed in H. pylori infection in humans and experimental models. Since the gastric epithelium undergoes rapid [...] Read more.
Helicobacter pylori is a leading cause of chronic gastric inflammation, generally associated with gastritis and adenocarcinoma. Activation of the NF-κB pathway mainly contributes to the inflammatory phenotype observed in H. pylori infection in humans and experimental models. Since the gastric epithelium undergoes rapid turnover, inflammation and pathogenicity of H. pylori result from early phase and chronically activated pathways. In the present study we investigated the early host response to H. pylori in non-tumoral human gastric epithelial cells (GES-1). To dissect the pathogen-specific mechanisms we also examined the response to tumor necrosis factor (TNF), a prototypical cytokine. By analyzing the activation state of NF-κB signaling, cytokine expression and secretion, and the transcriptome, we found that the inflammatory response of GES-1 cells to H. pylori and TNF results from activation of multiple pathways and transcription factors, e.g., NF-κB and CCAAT/enhancer-binding proteins (CEBPs). By comparing the transcriptomic profiles, we found that H. pylori infection induces a less potent inflammatory response than TNF but affects gene transcription to a greater extent by specifically inducing transcription factors such as CEBPβ and numerous zinc finger proteins. Our study provides insights on the cellular pathways modulated by H. pylori in non-tumoral human gastric cells unveiling new potential targets. Full article
(This article belongs to the Special Issue Exploring Molecular Mechanisms of Inflammatory Diseases)
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