Special Issue "Virulence Factors of Periodontal Pathogens: Secretion, Function and Interaction with Host Immune Responses"

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 5941

Special Issue Editors

Prof. Dr. Jan Potempa
E-Mail Website
Guest Editor
1. Department of Oral Immunity and Infectious Diseases, University of Louisville School of Dentistry, Louisville, KY, USA
2. Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland
Interests: proteolytic enzymes and their inhibitors in homeostasis and disease and molecular bases of virulence of periodontal pathogens and their relation to systemic diseases
Dr. Anna Maria Łasica
E-Mail Website
Guest Editor
Department of Bacterial Genetics, Institute of Microbiology, Faculty of Biology, University of Warsaw, Warsaw, Poland
Interests: enteropathogens; oral pathogens; molecular microbiology; T9SS; virulence

Special Issue Information

Dear Colleagues,

Recent methodological advances have accelerated research on periodontitis and the role of the dysbiotic microbiota on the tooth surface below the gum line in the development and maintenance of chronic inflammation of the periodontium. Concurrently, we have learned a lot about communication between bacteria recently in the dental plaque community and how they can corrupt host immune responses. Additionally, our knowledge of mechanisms causing erosion of the periodontium has increased exponentially. In all respects, Porphyromonas gingivalis, together with established and emerging periodontal pathogens, is at the center of the pathobiology of periodontitis. Therefore, the purpose of this Special Issue is to present major recent advances in investigations of different host and bacterial aspects of the disease emanating from several ground-braking findings in periodontal pathogens research in the last few years.

Potential topics include but are not limited to:

 (i) Structural and functional characterization of the novel type IX secretion system (T9SS) used by periodontal pathogens to secrete their proteinaceous virulence factors;

(ii) Advances in characterization of virulence factors structure on the atomic structure level; 

(iii) Understanding molecular mechanisms of dysbiotic community development on the tooth surface;

(iv) Elucidation of host signaling pathways manipulated by P. gingivalis and other periodontal pathogens;

(v) Implication of P. gingivalis as a potentially causative factor in diseases such as esophageal cancer, rheumatoid arthritis, Alzheimer’s disease, and other systemic diseases associated with periodontitis; 

(vi) Identification and characterization of new targets for development of novel strategies to prevent/treat periodontitis.

Such assembly of articles in one issue would be unique among the existing literature on oral pathogens and their role in pathogenesis of periodontitis and associated systemic diseases.

Prof. Dr. Jan Potempa
Dr. Anna Maria Łasica
Guest Editors

Manuscript Submission Information

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Keywords

  • periodontitis
  • T9SS
  • secretion
  • gingipains
  • therapy
  • cargo proteins
  • proteases
  • virulence factors
  • Porphyromonas gingivalis
  • Tannerella forsythia
  • Filifactor alocis
  • pathogenesis
  • host–pathogen interactions
  • innate immune system
  • complement
  • antigen
  • biofilm
  • dental plaque
  • oral pathogens

Published Papers (4 papers)

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Research

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Article
Proteomic Characterization of the Oral Pathogen Filifactor alocis Reveals Key Inter-Protein Interactions of Its RTX Toxin: FtxA
Pathogens 2022, 11(5), 590; https://doi.org/10.3390/pathogens11050590 - 17 May 2022
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Abstract
Filifactor alocis is a Gram-positive asaccharolytic, obligate anaerobic rod that has been isolated from a variety of oral infections including periodontitis, peri-implantitis, and odontogenic abscesses. As a newly emerging pathogen, its type strain has been investigated for pathogenic properties, yet little is known [...] Read more.
Filifactor alocis is a Gram-positive asaccharolytic, obligate anaerobic rod that has been isolated from a variety of oral infections including periodontitis, peri-implantitis, and odontogenic abscesses. As a newly emerging pathogen, its type strain has been investigated for pathogenic properties, yet little is known about its virulence variations among strains. We previously screened the whole genome of nine clinical oral isolates and a reference strain of F. alocis, and they expressed a novel RTX toxin, FtxA. In the present study, we aimed to use label-free quantification proteomics to characterize the full proteome of those ten F. alocis strains. A total of 872 proteins were quantified, and 97 among them were differentially expressed in FtxA-positive strains compared with the negative strains. In addition, 44 of these differentially expressed proteins formed 66 pairs of associations based on their predicted functions, which included clusters of proteins with DNA repair/mediated transformation and catalytic activity-related function, indicating different biosynthetic activities among strains. FtxA displayed specific interactions with another six intracellular proteins, forming a functional cluster that could discriminate between FtxA-producing and non-producing strains. Among them were FtxB and FtxD, predicted to be encoded by the same operon as FtxA. While revealing the broader qualitative and quantitative proteomic landscape of F. alocis, this study also sheds light on the deeper functional inter-relationships of FtxA, thus placing this RTX family member into context as a major virulence factor of this species. Full article
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Article
The Subgingival Plaque Microbiome, Systemic Antibodies against Bacteria and Citrullinated Proteins following Periodontal Therapy
Pathogens 2021, 10(2), 193; https://doi.org/10.3390/pathogens10020193 - 10 Feb 2021
Cited by 5 | Viewed by 2108
Abstract
Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation of anti-citrullinated protein antibodies (ACPAs) within [...] Read more.
Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation of anti-citrullinated protein antibodies (ACPAs) within susceptible hosts. Here, we sought to investigate whether periodontal treatment influenced systemic inflammation and antibody titres to P. gingivalis, A. actinomycetemcomitans, Prevotella intermedia and ACPA in 42 systemically health patients with periodontal disease. Subgingival plaque and serum samples were collected from study participants before (baseline) and 90 days after treatment to analyse the abundance of specific bacteria and evaluate anti-bacterial antibodies, C-reactive protein (CRP), tumour necrosis factor α (TNF-α), interleukin 6 (IL-6) and ACPA in serum. Following treatment, all patients showed reduced periodontal inflammation. Despite observing a weak positive correlation between CRP and IL-6 with periodontal inflammation at baseline, we observed no significant reductions in any indicators of systemic inflammation 90 days after treatment. In contrast, anti-P. gingivalis IgG significantly reduced post-treatment (p < 0.001, Wilcoxon signed rank test), although no changes were observed for other antibody titres. Patients who had detectable P. gingivalis in subgingival plaques had significantly higher anti-P. gingivalis IgG and ACPA titres, suggesting a potential association between P. gingivalis colonisation and systemic antibody titres. Full article
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Article
Application of the In Vitro HoxB8 Model System to Characterize the Contributions of Neutrophil–LPS Interaction to Periodontal Disease
Pathogens 2020, 9(7), 530; https://doi.org/10.3390/pathogens9070530 - 01 Jul 2020
Viewed by 1694
Abstract
(1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such as functional deficiency or a lack [...] Read more.
(1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such as functional deficiency or a lack of expression of surface markers characteristic of neutrophils. P. gingivalis is a periodontopathogen that causes dysbiosis in subgingival bacterial biofilm. This triggers the accumulation of functional neutrophils in the periodontium. However, until now, the specific effects of P. gingivalis-derived lipopolysaccharide on neutrophil functions have not been analyzed. (2) Methods: The impact of two variants of commercially available P. gingivalis endotoxin on neutrophil functions was tested using the HoxB8 in vitro system that is well suited to analyze neutrophil response to different stimuli in a controlled manner. (3) Results: The Standard P. gingivalis lipopolysaccharide (LPS), known to activate cells through Toll-like receptor 2 (TLR2)- and Toll-like receptor 4 (TLR4)-dependent pathways, prolonged neutrophil survival and exhibited pro-inflammatory effects. In contrast, Ultrapure LPS, binding exclusively to TLR4, neither protected neutrophils from apoptosis, nor induced an inflammatory response. (4) Conclusion: Two variants of P. gingivalis-derived LPS elicited effects on neutrophils and, based on the obtained results, we concluded that the engagement of both TLR2 and TLR4 is required for the manipulation of survival and the stimulation of immune responses of HoxB8 neutrophils. Full article
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Review

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Review
A Tale of Two Fimbriae: How Invasion of Dendritic Cells by Porphyromonas gingivalis Disrupts DC Maturation and Depolarizes the T-Cell-Mediated Immune Response
Pathogens 2022, 11(3), 328; https://doi.org/10.3390/pathogens11030328 - 08 Mar 2022
Cited by 1 | Viewed by 685
Abstract
Porphyromonas gingivalis (P. gingivalis) is a unique pathogen implicated in severe forms of periodontitis (PD), a disease that affects around 50% of the US population. P. gingivalis is equipped with a plethora of virulence factors that it uses to exploit its [...] Read more.
Porphyromonas gingivalis (P. gingivalis) is a unique pathogen implicated in severe forms of periodontitis (PD), a disease that affects around 50% of the US population. P. gingivalis is equipped with a plethora of virulence factors that it uses to exploit its environment and survive. These include distinct fimbrial adhesins that enable it to bind to other microbes, colonize inflamed tissues, acquire nutrients, and invade cells of the stroma and immune system. Most notable for this review is its ability to invade dendritic cells (DCs), which bridge the innate and adaptive immune systems. This invasion process is tightly linked to the bridging functions of resultant DCs, in that it can disable (or stimulate) the maturation function of DCs and cytokines that are secreted. Maturation molecules (e.g., MHCII, CD80/CD86, CD40) and inflammatory cytokines (e.g., IL-1b, TNFa, IL-6) are essential signals for antigen presentation and for proliferation of effector T-cells such as Th17 cells. In this regard, the ability of P. gingivalis to coordinately regulate its expression of major (fimA) and minor (mfa-1) fimbriae under different environmental influences becomes highly relevant. This review will, therefore, focus on the immunoregulatory role of P. gingivalis fimbriae in the invasion of DCs, intracellular signaling, and functional outcomes such as alveolar bone loss and immune senescence. Full article
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