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Pathogens
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Aggregatibacter actinomycetemcomitans
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Aggregatibacter actinomycetemcomitans

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Bacterial Pathogens".

Deadline for manuscript submissions: 20 May 2024 | Viewed by 2519

Special Issue Editor

Prof. Dr. Daniel H. Fine

E-Mail Website
Guest Editor
Department of Oral Biology, School of Dental Medicine, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA
Interests: microbial genetics; pathogenesis; Aggregatibacter actinomycetemcomitans; periodontal disease etiology; host/pathogen interactions

Special Issue Information

Dear Colleagues,

Aggregatibacter actinomycetemcomitans is a Gram-negative bacterium associated with localized aggressive periodontitis. It is equipped with several potent virulence factors that can cause cell death and induce or evade inflammation. However, research on its pathogenic mechanism in the human body and preclinical experimental models are still in the process of dynamic exploration.

The focus of this Special Issue is on the following three research directions related to A. actinomycetemcomitans:

(1) Aggregatibacter actinomycetemcomitans and its relationship to periodontal disease and other clinical infections;
(2) Aggregatibacter actinomycetemcomitans virulence genes;
(3) Aggregatibacter actinomycetemcomitans and ecological relationships in supra- and subgingival biofilms.

Prof. Dr. Daniel H. Fine
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. Pathogens 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

  • Aggregatibacteria actinomycetemcomitans
  • periodontal pathogen
  • virulence mechanisms
  • periodontitis
  • leukotoxin
  • cytolethal distending toxin
  • epidemiology
  • collagenase
  • periodontal disease etiology
  • biofilm

Published Papers (4 papers)

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Research

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11 pages, 434 KiB  
Article
Presence and Immunoreactivity of Aggregatibacter actinomycetemcomitans in Rheumatoid Arthritis
by Anna Svärd, Riccardo LoMartire, Klara Martinsson, Carina Öhman, Alf Kastbom and Anders Johansson
Pathogens 2024, 13(5), 368; https://doi.org/10.3390/pathogens13050368 (registering DOI) - 29 Apr 2024
Abstract
The presence of periodontal pathogens is associated with an increased prevalence of rheumatoid arthritis (RA). The systemic antibody response to epitopes of these bacteria is often used as a proxy to study correlations between bacteria and RA. The primary aim of the present [...] Read more.
The presence of periodontal pathogens is associated with an increased prevalence of rheumatoid arthritis (RA). The systemic antibody response to epitopes of these bacteria is often used as a proxy to study correlations between bacteria and RA. The primary aim of the present study is to examine the correlation between the presence of Aggregatibacter actinomycetemcomitans (Aa) in the oral cavity and serum antibodies against the leukotoxin (LtxA) produced by this bacterium. The salivary presence of Aa was analyzed with quantitative PCR and serum LtxA ab in a cell culture-based neutralization assay. The analyses were performed on samples from a well-characterized RA cohort (n = 189) and a reference population of blood donors (n = 101). Salivary Aa was present in 15% of the RA patients and 6% of the blood donors. LtxA ab were detected in 19% of RA-sera and in 16% of sera from blood donors. The correlation between salivary Aa and serum LtxA ab was surprisingly low (rho = 0.55 [95% CI: 0.40, 0.68]). The presence of salivary Aa showed no significant association with any of the RA-associated parameters documented in the cohort. A limitation of the present study is the relatively low number of individuals with detectable concentrations of Aa in saliva. Moreover, in the comparison of detectable Aa prevalence between RA patients and blood donors, we assumed that the two groups were equivalent in other Aa prognostic factors. These limitations must be taken into consideration when the result from the study is interpreted. We conclude that a systemic immune response to Aa LtxA does not fully reflect the prevalence of Aa in saliva. In addition, the association between RA-associated parameters and the presence of Aa was negligible in the present RA cohort. Full article
(This article belongs to the Special Issue Aggregatibacter actinomycetemcomitans)
19 pages, 1966 KiB  
Article
Aggregatibacter actinomycetemcomitans Cytolethal Distending Toxin Induces Cellugyrin-(Synaptogyrin 2) Dependent Cellular Senescence in Oral Keratinocytes
by Bruce J. Shenker, Jonathan Korostoff, Lisa P. Walker, Ali Zekavat, Anuradha Dhingra, Taewan J. Kim and Kathleen Boesze-Battaglia
Pathogens 2024, 13(2), 155; https://doi.org/10.3390/pathogens13020155 - 08 Feb 2024
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Abstract
Recently, we reported that oral-epithelial cells (OE) are unique in their response to Aggregatibacter actinomycetemcomitans cytolethal distending toxin (Cdt) in that cell cycle arrest (G2/M) occurs without leading to apoptosis. We now demonstrate that Cdt-induced cell cycle arrest in OE has a duration [...] Read more.
Recently, we reported that oral-epithelial cells (OE) are unique in their response to Aggregatibacter actinomycetemcomitans cytolethal distending toxin (Cdt) in that cell cycle arrest (G2/M) occurs without leading to apoptosis. We now demonstrate that Cdt-induced cell cycle arrest in OE has a duration of at least 7 days with no change in viability. Moreover, toxin-treated OE develops a new phenotype consistent with cellular senescence; this includes increased senescence-associated β-galactosidase (SA-β-gal) activity and accumulation of the lipopigment, lipofuscin. Moreover, the cells exhibit a secretory profile associated with cellular senescence known as the senescence-associated secretory phenotype (SASP), which includes IL-6, IL-8 and RANKL. Another unique feature of Cdt-induced OE senescence is disruption of barrier function, as shown by loss of transepithelial electrical resistance and confocal microscopic assessment of primary gingival keratinocyte structure. Finally, we demonstrate that Cdt-induced senescence is dependent upon the host cell protein cellugyrin, a homologue of the synaptic vesicle protein synaptogyrin. Collectively, these observations point to a novel pathogenic outcome in oral epithelium that we propose contributes to both A. actinomycetemcomitans infection and periodontal disease progression. Full article
(This article belongs to the Special Issue Aggregatibacter actinomycetemcomitans)
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Review

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11 pages, 1569 KiB  
Review
Therapeutic Applications of Aggregatibacter actinomycetemcomitans Leukotoxin
by Scott C. Kachlany and Brian A. Vega
Pathogens 2024, 13(5), 354; https://doi.org/10.3390/pathogens13050354 (registering DOI) - 25 Apr 2024
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Abstract
Aggregatibacter actinomycetemcomitans is a Gram-negative oral bacterium that has been primarily studied for its role in causing periodontal disease. The bacterium has also been implicated in several systemic diseases such as endocarditis and soft tissue abscesses. Leukotoxin (LtxA) is perhaps the best studied [...] Read more.
Aggregatibacter actinomycetemcomitans is a Gram-negative oral bacterium that has been primarily studied for its role in causing periodontal disease. The bacterium has also been implicated in several systemic diseases such as endocarditis and soft tissue abscesses. Leukotoxin (LtxA) is perhaps the best studied protein virulence factor from A. actinomycetemcomitans. The protein can rapidly destroy white blood cells (WBCs), helping the bacterium to subvert the host immune system. The functional receptor for LtxA is lymphocyte function associated antigen-1 (LFA-1), which is expressed exclusively on the surfaces of WBCs. Bacterial expression and secretion of the protein are highly regulated and controlled by a number of genetic and environmental factors. The mechanism of LtxA action on WBCs varies depending on the type of cell that is being killed, and the protein has been shown to activate numerous cell death pathways in susceptible cells. In addition to serving as an important virulence factor for the bacterium, because of its exquisite specificity and rapid activity, LtxA is also being investigated as a therapeutic agent that may be used to treat diseases such as hematological malignancies and autoimmune/inflammatory diseases. It is our hope that this review will inspire an increased intensity of research related to LtxA and its effect on Aggressive Periodontitis, the disease that led to its initial discovery. Full article
(This article belongs to the Special Issue Aggregatibacter actinomycetemcomitans)
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19 pages, 3769 KiB  
Review
The Trimeric Autotransporter Adhesin EmaA and Infective Endocarditis
by Keith P. Mintz, David R. Danforth and Teresa Ruiz
Pathogens 2024, 13(2), 99; https://doi.org/10.3390/pathogens13020099 - 23 Jan 2024
Viewed by 1011
Abstract
Infective endocarditis (IE), a disease of the endocardial surface of the heart, is usually of bacterial origin and disproportionally affects individuals with underlying structural heart disease. Although IE is typically associated with Gram-positive bacteria, a minority of cases are caused by a group [...] Read more.
Infective endocarditis (IE), a disease of the endocardial surface of the heart, is usually of bacterial origin and disproportionally affects individuals with underlying structural heart disease. Although IE is typically associated with Gram-positive bacteria, a minority of cases are caused by a group of Gram-negative species referred to as the HACEK group. These species, classically associated with the oral cavity, consist of bacteria from the genera Haemophilus (excluding Haemophilus influenzae), Aggregatibacter, Cardiobacterium, Eikenella, and Kingella. Aggregatibacter actinomycetemcomitans, a bacterium of the Pasteurellaceae family, is classically associated with Aggressive Periodontitis and is also concomitant with the chronic form of the disease. Bacterial colonization of the oral cavity serves as a reservoir for infection at distal body sites via hematological spreading. A. actinomycetemcomitans adheres to and causes disease at multiple physiologic niches using a diverse array of bacterial cell surface structures, which include both fimbrial and nonfimbrial adhesins. The nonfimbrial adhesin EmaA (extracellular matrix binding protein adhesin A), which displays sequence heterogeneity dependent on the serotype of the bacterium, has been identified as a virulence determinant in the initiation of IE. In this chapter, we will discuss the known biochemical, molecular, and structural aspects of this protein, including its interactions with extracellular matrix components and how this multifunctional adhesin may contribute to the pathogenicity of A. actinomycetemcomitans. Full article
(This article belongs to the Special Issue Aggregatibacter actinomycetemcomitans)
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