Mixed anaerobic thoracic empyema: the first report of Filifactor alocis causing extra-oral disease

Gray, Robert M.; Vidwans, M A

doi:10.1016/j.nmni.2019.100528

Cited by 13 publications

(8 citation statements)

References 16 publications

(17 reference statements)

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“…For example, P. gingivalis 16S rRNAs were detected in Alzheimer’s disease brains, suggesting their passage through the blood‐brain barrier, as well as in the synovial fluid of patients with rheumatoid arthritis (Arana et al, 2018; Dominy et al, 2019). Interestingly, two recent reports identified F. alocis at extra‐oral sites, in patients with lung cancer and chronic dysphagia (Gray & Vidwans, 2019; Wang et al, 2019). It is possible that components of oral bacteria found at distal sites were mediated by EVs.…”

Section: Discussionmentioning

confidence: 99%

Filifactor alocis‐derived extracellular vesicles inhibit osteogenesis through TLR2 signaling

Song

Kim

Choi

et al. 2020

Molecular Oral Microbiology

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Periodontitis is a prevalent microbial-induced infectious disease. It induces chronic inflammation and results in destruction of connective tissue such as gingiva and periodontal ligaments as well the alveolar bone supporting teeth. Severe periodontitis is the sixth most common disease worldwide, affecting 734 million people with an overall prevalence of 11.2% (Richards, 2014). Its incidence is also associated with systemic disease such as osteoporosis, cardiovascular disease, adverse pregnancy outcomes, rheumatoid arthritis, and Alzheimer's disease (Hajishengallis, 2015), a factor that has promoted research into the pathogenesis and influence of oral pathogens on the body. Filifactor alocis, an asaccharolytic anaerobic Gram-positive rod (AAGPR), is a marker organism of periodontal disease such as periodontitis, peri-implantitis, and apical periodontitis (Aruni, Chioma, & Fletcher, 2014). The environments surrounding the periapical region and the periodontal pocket in periodontitis patients are well-suited for F. alocis as a result of the characteristics of AAGPRs. F. alocis is a prevalent pathogen in periodontitis that is infrequently detected in healthy or periodontitis-resistant patients (Kumar et al., 2003). The pathogenicity of F. alocis is indicated by an associated increase in neutrophil recruitment and inflammatory cytokines (Armstrong et al., 2016; Vashishta et al., 2019; Wang et al., 2014). F. alocis also induces apoptosis of epithelial cells and keratinocytes via caspase activation and increases cyclooxygenase; cyclooxygenase is responsible for the production of PGE2, which is involved in tissue damage and osteoclastic bone resorption in HGF-1 and THP-1 cells (Chioma,

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Section: Discussionmentioning

confidence: 99%

Filifactor alocis‐derived extracellular vesicles inhibit osteogenesis through TLR2 signaling

Song

Kim

Choi

et al. 2020

Molecular Oral Microbiology

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“…Consistent with this study, 2 recent reports identified F. alocis at extraoral sites in association with a disease other than periodontitis. The first case report identified F. alocis in the pleural fluid of a patient with thoracic empyema, whereas in the second report, the bacterium was found in the fluid bronchoalveolar lavage of patients with lung cancer (Gray and Vidwans 2019; Wang et al 2019). Additionally, F. alocis has been identified in brain abscesses (Hishiya et al 2020) and shown to aid progression of periodontitis in patients with rheumatoid arthritis (Ayala Herrera et al 2019).…”

Section: F Alocis: Prevalence and Characteristicsmentioning

confidence: 99%

Filifactor alocis: Recent Insights and Advances

et al. 2021

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Filifactor alocis, a fastidious Gram-positive obligate anaerobic bacterium, is a newly appreciated member of the periodontal community that is now proposed to be a diagnostic indicator of periodontal disease. Its pathogenic characteristics are highlighted by its ability to survive in the oxidative stress–rich environment of the periodontal pocket and to significantly alter the microbial community dynamics by forming biofilms and interacting with several oral bacteria. Here, we describe the current understanding of F. alocis virulence attributes, such as its comparative resistance to oxidative stress, production of unique proteases and collagenases that can cause structural damage to host cells, and dysregulation of the immune system, which enable this bacterium to colonize, survive, and outcompete other traditional pathogens in the inflammatory environment of the periodontal pocket. Furthermore, we explore the recent advancements and future directions for F. alocis research, including the potential mechanisms for oxidative stress resistance and our evolving understanding of the interactions and mechanisms of bacterial survival inside neutrophils. We also discuss the current genetic tools and challenges involved in manipulating the F. alocis genome for the functional characterization of the putative virulence genes. Collectively, this information will expedite F. alocis research and should lead to the identification of prime targets for the development of novel therapeutics to aid in the control and prevention of periodontal disease.

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“…In patients with aggressive periodontitis, the presence of F. alocis with A. actinomycetemcomitans and Streptococcus parasanguinis in subgingival tissue is closely associated with bone loss (Fine et al, 2013). F. alocis was also found in extraoral sites such as brain abscesses (Hishiya et al, 2020) and thoracic empyema (Gray and Vidwans, 2019). F. alocis infections are characterized by the dysfunctional modulation of neutrophils (Edmisson et al, 2018), adhesion to and invasion of epithelial cells, resistance to oxidative stress (Aruni et al, 2011), and inhibition of complement cascades (Jusko et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Extracellular vesicles derived from the periodontal pathogen Filifactor alocis induce systemic bone loss through Toll‐like receptor 2

Kim

Song

Gho

et al. 2021

J of Extracellular Vesicle

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Periodontitis is an inflammatory disease induced by local infection in toothsupporting tissue. Periodontitis is associated with systemic bone diseases, but little is known about the mechanism of the causal effect of periodontitis on systemic bone resorption. Bacteria-derived extracellular vesicles (EVs) act as natural carriers of virulence factors that are responsible for systemic inflammation. In this study, we investigated the role of EVs derived from Filifactor alocis, a Gram-positive, anaerobic periodontal pathogen, in systemic bone loss and osteoclast differentiation. F. alocis EVs accumulated in the long bones of mice after intraperitoneal administration. These EVs induced proinflammatory cytokines, osteoclastogenesis, and bone resorption via Toll-like receptor 2 (TLR2). The phase separation of F. alocis EVs showed that amphiphilic molecules were responsible for the induced bone resorption and osteoclastogenesis. The osteoclastogenic effects of F. alocis EVs were reduced by lipoprotein lipase. Proteomic analysis of the amphiphilic molecules identified seven lipoproteins. Our results indicate that lipoprotein-like molecules in F. alocis EVs may contribute to systemic bone loss via TLR2.

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Mixed anaerobic thoracic empyema: the first report of Filifactor alocis causing extra-oral disease

Abstract: We report on a case of bilateral lung consolidation and thoracic empyema caused by the periodontal pathogens Filifactor alocis and Campylobacter rectus in a patient with chronic dysphagia. This is the first report of Filifactor alocis causing infection at an extra-oral site.

Cited by 13 publications

References 16 publications

Filifactor alocis‐derived extracellular vesicles inhibit osteogenesis through TLR2 signaling

Filifactor alocis‐derived extracellular vesicles inhibit osteogenesis through TLR2 signaling

Filifactor alocis: Recent Insights and Advances

Extracellular vesicles derived from the periodontal pathogen Filifactor alocis induce systemic bone loss through Toll‐like receptor 2

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