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Microorganisms
Special Issues
Microbial Infections and Rheumatic Diseases
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Microbial Infections and Rheumatic Diseases

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: 15 June 2024 | Viewed by 6037

Special Issue Editors

Dr. Rossella Talotta

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, Rheumatology Unit, AOU “Gaetano Martino”, University of Messina, 98100 Messina, Italy
Interests: Immunology; Rheumatology; Pharmacology; Bioinformatics; Molecular Biology; Immunogenicity, Biomarkers
Jacopo Angelini

E-Mail Website
Guest Editor Assistant
Clinical Pharmacology and Toxicology Institute, University Hospital Friuli Centrale ASU FC, 33100 Udine, Italy
Interests: pharmacology

Special Issue Information

Dear Colleagues,

It gives us great pleasure to present this Special Issue, which deals with host–pathogen interactions in the development of rheumatic diseases, and the pharmacological aspects involved. The idea that the disruption of the delicate balance between host and microorganisms can lead to rheumatologic diseases has been deciphered since the beginning of the last century. Emblematic examples are the postinfectious sequelae of group A streptococci and reactive arthritis following bacterial gastrointestinal or urogenital infections. More recently, novel microbial agents, including SARS-CoV-2, pathobionts, and endogenous retroviruses, have been included among the potential candidates responsible for the onset or flare-up of immune-mediated disorders. In addition, the rapid development of biomolecular and computational technologies has enabled researchers to unravel novel pathogenic mechanisms linking microbial infections to rheumatic diseases, including osteoporosis and osteoarthritis. Accordingly, drugs used in rheumatology have been characterized in terms of their antimicrobial activity, while on the other hand, research on the appropriate use of antimicrobial agents in these patients continues.

This Special Issue brings together the most innovative research data on this topic, focusing on new biomolecular or bioinformatics discoveries on common or atypical infections and coinfections affecting autoimmunity, as well as associated pathogenic mechanisms (e.g., epigenetics, molecular mimicry, bystander activation, or cryptic antigen formation), the role of microbes in combating rheumatic diseases, and pharmacological aspects (e.g., appropriate management, pharmacokinetics, pharmacodynamics, and drug–drug interactions in patients treated with antirheumatic and antimicrobial agents, including vaccines). Research articles, short communications, reviews, and mini-reviews are welcome.

Dr. Rossella Talotta
Guest Editor

Jacopo Angelini
Guest Editor Assistant

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. Microorganisms 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 2700 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

  • rheumatic diseases
  • microorganisms
  • host–pathogen interaction
  • dysbiosis
  • antibiotics
  • prebiotics
  • probiotics
  • vaccines
  • biomarkers
  • drug–drug interaction

Published Papers (3 papers)

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Research

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19 pages, 794 KiB  
Article
Molecular Mimicry and HLA Polymorphisms May Drive Autoimmunity in Recipients of the BNT-162b2 mRNA Vaccine: A Computational Analysis
by Rossella Talotta
Microorganisms 2023, 11(7), 1686; https://doi.org/10.3390/microorganisms11071686 - 28 Jun 2023
Cited by 3 | Viewed by 1449
Abstract
Background: After the start of the worldwide COVID-19 vaccination campaign, there were increased reports of autoimmune diseases occurring de novo after vaccination. This in silico analysis aimed to investigate the presence of protein epitopes encoded by the BNT-162b2 mRNA vaccine, one of the [...] Read more.
Background: After the start of the worldwide COVID-19 vaccination campaign, there were increased reports of autoimmune diseases occurring de novo after vaccination. This in silico analysis aimed to investigate the presence of protein epitopes encoded by the BNT-162b2 mRNA vaccine, one of the most widely administered COVID-19 vaccines, which could induce autoimmunity in predisposed individuals. Methods: The FASTA sequence of the protein encoded by the BNT-162b2 vaccine served as the key input to the Immune Epitope Database and Analysis Resource. Linear peptides with 90% BLAST homology were selected, and T-cell, B-cell, and MHC-ligand assays without MHC restriction were searched and analyzed. HLA disease associations were screened on the HLA-SPREAD platform by selecting only positive markers. Results: By 7 May 2023, a total of 5693 epitopes corresponding to 21 viral but also human proteins were found. The latter included CHL1, ENTPD1, MEAF6, SLC35G2, and ZFHX2. Importantly, some autoepitopes may be presented by HLA alleles positively associated with various immunological diseases. Conclusions: The protein product of the BNT-162b2 mRNA vaccine contains immunogenic epitopes that may trigger autoimmune phenomena in predisposed individuals through a molecular mimicry mechanism. Genotyping for HLA alleles may help identify individuals at risk. However, further wet-lab studies are needed to confirm this hypothesis. Full article
(This article belongs to the Special Issue Microbial Infections and Rheumatic Diseases)
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15 pages, 2087 KiB  
Article
Expression of Envelope Protein Encoded by Endogenous Retrovirus K102 in Rheumatoid Arthritis Neutrophils
by Amanda Laine, Xiaoxing Wang, Kathryn Ni, Sarah E. B. Smith, Rayan Najjar, Leanne S. Whitmore, Michael Yacoub, Alison Bays, Michael Gale, Jr. and Tomas Mustelin
Microorganisms 2023, 11(5), 1310; https://doi.org/10.3390/microorganisms11051310 - 17 May 2023
Cited by 1 | Viewed by 1624
Abstract
Many patients suffering from autoimmune diseases have autoantibodies against proteins encoded by genomic retroelements, suggesting that normal epigenetic silencing is insufficient to prevent the production of the encoded proteins for which immune tolerance appears to be limited. One such protein is the transmembrane [...] Read more.
Many patients suffering from autoimmune diseases have autoantibodies against proteins encoded by genomic retroelements, suggesting that normal epigenetic silencing is insufficient to prevent the production of the encoded proteins for which immune tolerance appears to be limited. One such protein is the transmembrane envelope (Env) protein encoded by human endogenous retrovirus K (HERV-K). We reported recently that patients with rheumatoid arthritis (RA) have IgG autoantibodies that recognize Env. Here, we use RNA sequencing of RA neutrophils to analyze HERV-K expression and find that only two loci with an intact open-reading frame for Env, HERV-K102, and K108 are expressed, but only the former is increased in RA. In contrast, other immune cells express more K108 than K102. Patient autoantibodies recognized endogenously expressed Env in breast cancer cells and in RA neutrophils but not healthy controls. A monoclonal anti-Env antibody also detected Env on the surface of RA neutrophils but very little on the surface of other immune cells. We conclude that HERV-K102 is the locus that produces Env detectable on the surface of neutrophils in RA. The low levels of HERV-K108 transcripts may contribute only marginally to cell surface Env on neutrophils or other immune cells in some patients. Full article
(This article belongs to the Special Issue Microbial Infections and Rheumatic Diseases)
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Review

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15 pages, 563 KiB  
Review
Autoimmunity and Infection in Glomerular Disease
by Chiara Casuscelli, Elisa Longhitano, Veronica Maressa, Silvia Di Carlo, Luigi Peritore, Simone Di Lorenzo, Vincenzo Calabrese, Valeria Cernaro and Domenico Santoro
Microorganisms 2023, 11(9), 2227; https://doi.org/10.3390/microorganisms11092227 - 2 Sep 2023
Cited by 1 | Viewed by 1545
Abstract
The ongoing glomerular damage of infections is not limited to the most widely known form of post-streptococcal glomerulonephritis, which is today less common in the Western world; other forms of glomerulonephritis are associated with several bacterial, viral and parasitic pathogens. The mechanisms responsible [...] Read more.
The ongoing glomerular damage of infections is not limited to the most widely known form of post-streptococcal glomerulonephritis, which is today less common in the Western world; other forms of glomerulonephritis are associated with several bacterial, viral and parasitic pathogens. The mechanisms responsible range from the direct damage of glomerular cells to the formation and deposition of immunocomplexes to molecular mimicry to the secretion of superantigens. Similarly, in the course of glomerular disease, infections are more frequent than in the general population due to the loss of immunoglobulins in urine and the immunosuppressive agents used to treat the autoimmune disease that decrease the activity of the immune system. Recognizing this two-way link, understanding its pathogenetic mechanism, and identifying the most appropriate therapeutic choice are essential for the personalized management of patients. In this continuously developing field, this short review summarizes the current state of the art as support for physicians, who are increasingly involved in managing patients with glomerular disease and infections. Full article
(This article belongs to the Special Issue Microbial Infections and Rheumatic Diseases)
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