ArticleMolecular oral microbiology2017
Filifactor alocis collagenase can modulate apoptosis of normal oral keratinocytes.
Article in Molecular oral microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Increased bacterial load ofFrontiers in oral health · 2025Article
- DAMPs and alarmin gene expression patterns in aging healthy and diseased mucosal tissues.Frontiers in oral health · 2023Article
- The emerging oral pathogen, Filifactor alocis, extends the functional lifespan of human neutrophils.Molecular microbiology · 2022Article
- Regulation of olfactomedin 4 by Porphyromonas gingivalis in a community context.The ISME journal · 2021Article
- Article
- Regulation of matrix metalloproteinase-1 by Filifactor alocis in human gingival and monocytic cells.Clinical oral investigations · 2020Article
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Authors and funding
4 authors.
Funding
Abstract
To successfully colonize host cells, pathogenic bacteria must circumvent the host's structural barrier such as the collagen-rich extracellular matrix (ECM), as a preliminary step to invasion and colonization of the periodontal tissue. Filifactor alocis possesses a putative Peptidase U32 family protein (HMPREF0389_00504) with collagenase activity that may play a significant role in colonization of host tissue during periodontitis by breaking down collagen into peptides and disruption of the host cell. Domain architecture of the HMPREF0389_00504 protein predicted the presence of a characteristic PrtC-like collagenase domain, and a peptidase domain. Our study demonstrated that the recombinant F. alocis peptidase U32 protein (designated PrtFAC) can interact with, and degrade, type I collagen, heat-denatured collagen and gelatin in a calcium-dependent manner. PrtFAC decreased viability and induced apoptosis of normal oral keratinocytes (NOKs) in a time and dose-dependent manner. Transcriptome analysis of NOK cells treated with PrtFAC showed an upregulation of the genes encoding human pro-apoptotic proteins: Apoptotic peptidase activating factor 1 (Apaf1) cytochrome C, as well as caspase 3 and caspase 9, suggesting the involvement of the mitochondrial apoptotic pathway. There was a significant increase in caspase 3/7 activity in NOK cells treated with PrtFAC. Taken together, these findings suggest that F. alocis PrtFAC protein may play a role in the virulence and pathogenesis of F. alocis.
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