Global changes in human neutrophil transcriptome profile during Filifactor alocis challenge
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ABSTRACT:
PROVIDER: PRJNA565218 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10106400.fastq.gz | Fastqsanger.gz | |||
| SRR10106401.fastq.gz | Fastqsanger.gz | |||
| SRR10106402.fastq.gz | Fastqsanger.gz | |||
| SRR10106403.fastq.gz | Fastqsanger.gz | |||
| SRR10106404.fastq.gz | Fastqsanger.gz |
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Project description:Periodontitis is a multifactorial chronic inflammatory infectious disease with a high prevalence in the adult population in the USA. Until recently, research into periodontitis focused primarily on putative pathogens such as Porphyromonas gingivalis. However, a reappraisal of microbial etiology has marked a turning point in the field due to the development of culture-independent techniques that allow the identification of bacterial species directly from nucleic acids. Filifactor alocis, a Gram positive anaerobic oral bacterium, has emerged as an important periodontal pathogen. Neutrophils are recruited in high numbers to the gingival tissue, where they are linked with protection against periodontal disease. However, periodontal pathogens evolved different strategies to resist neutrophil microbicidal mechanisms while propagating inflammation, which affords a source of nutrients. The goal of this study was to determine the global changes in human neutrophil gene expression induced by F. alocis challenge. RNA-sequencing analysis shows that F. alocis-challenge alters human neutrophil transcriptome including expression of genes associated with regulation of Toll-Like Receptor signaling pathway, MAPK signaling pathway, apoptosis, cytokines and chemokines, among other neutrophil effector functions.
2020-04-06 | GSE137351 | GEO
Project description:We use high through put RNA sequenceing technology to study the genome-wide expression profile in an oral pathogen Filifactor alocis when co-cultured with another key-stone oral pathogen Porphyromonas gingivalis under anaerobic conditions and oxidative stress conditions.
2021-08-13 | GSE181879 | GEO
Project description:Tobacco Smoke Exacerbates Filifactor alocis Pathogenicity
| PRJNA870570 | ENA
Project description:Filifactor alocis is a Gram-positive asaccharolytic, obligate anaerobic rod of the phylum Firmicutes, strongly associated with periodontitis. In this study, we performed the whole proteomic analysis of an F. alocis type strain (ATCC 35896; CCUG 47790), as well as nine clinically isolated strains at the Clinical Oral Microbiology Laboratory, Umeå University, for identification and deeper characterization of this species. Label-free quantification was used to compare the proteomic differences between different strains.
2022-06-09 | PXD026971 | Pride
Project description:Oal anaerobic bacteria have to face constant oxidative stress in order to survive in the inflammatory environment of the periodontal pocket. In this study, we analyzed the transcriptome profiles of P. gingivalis and Filifactor in monoculture as compared to P. gingivalis+F.alocis coculture under H2O2 stress condtions, to analyze the genes responsible for enhanced survival of P. gingivalis in presence of F. alocis under oxidative-stress conditions.
2023-09-01 | GSE241660 | GEO
Project description:Transcriptome analysis of Filifactor alocis in co-culture with Porphyromonas gingivalis
| PRJNA753797 | ENA
Project description:Filifactor alocis is a newly appreciated pathogen in periodontal diseases. Neutrophils are the predominant innate immune cell in the gingival crevice. In this study, we examined modulation of human neutrophil antimicrobial functions by F. alocis. Both non-opsonised and serum-opsonised F. alocis were engulfed by neutrophils but were not efficiently eliminated. Challenge of neutrophils with either non-opsonised or serum-opsonised F. alocis induced a minimal intracellular as well as extracellular respiratory burst response compared to opsonised Staphylococcus aureus and fMLF, respectively. However, pretreatment or simultaneous challenge of neutrophils with F. alocis did not affect the subsequent oxidative response to a particulate stimulus, suggesting that the inability to trigger the respiratory response was only localised to F. alocis phagosomes. In addition, although neutrophils engulfed live or heat-killed F. alocis with the same efficiency, heat-killed F. alocis elicited a higher intracellular respiratory burst response compared to viable organisms, along with decreased surface expression of CD35, a marker of secretory vesicles. F. alocis phagosomes remained immature by delayed and reduced recruitment of specific and azurophil granules, respectively. These results suggest that F. alocis withstands neutrophil antimicrobial responses by preventing intracellular ROS production, along with specific and azurophil granule recruitment to the bacterial phagosome.
| S-EPMC5980721 | biostudies-literature
Project description:BackgroundBacteria in periodontal pockets develop complex sessile communities that attach to the tooth surface. These highly dynamic microfloral environments challenge both clinicians and researchers alike. The exploration of structural organisation and bacterial interactions within these biofilms is critically important for a thorough understanding of periodontal disease. In recent years, Filifactor alocis, a fastidious, Gram-positive, obligately anaerobic rod was repeatedly identified in periodontal lesions using DNA-based methods. It has been suggested to be a marker for periodontal deterioration. The present study investigated the epidemiology of F. alocis in periodontal pockets and analysed the spatial arrangement and architectural role of the organism in in vivo grown subgingival biofilms.ResultsA species-specific oligonucleotide probe, FIAL, was designed and evaluated. A total of 490 subgingival plaque samples were submitted to PCR and subsequent dot blot hybridization to compare the prevalence of F. alocis in patients suffering from generalized aggressive periodontitis (GAP), chronic periodontitis (CP), and control subjects resistant to periodontitis. Moreover, a specially designed carrier system was used to collect in vivo grown subgingival biofilms from GAP patients. Subsequent topographic analysis was performed using fluorescence in situ hybridization.While the majority of patients suffering from GAP or CP harboured F. alocis, it was rarely detected in the control group. In the examined carrier-borne biofilms the organism predominantly colonized apical parts of the pocket in close proximity to the soft tissues and was involved in numerous structures that constitute characteristic architectural features of subgingival periodontal biofilms.ConclusionsF. alocis is likely to make a relevant contribution to the pathogenetic structure of biofilms accounting for periodontal inflammation and can be considered an excellent marker organism for periodontal disease.
| S-EPMC2846919 | biostudies-literature
Project description:AimFilifactor alocis has recently emerged as a periodontal pathobiont that appears to thrive in the oral cavity of smokers. We hypothesized that identification of smoke-responsive F. alocis genes would provide insight into adaptive strategies and that cigarette smoke would enhance F. alocis pathogenesis in vivo.Materials and methodsF. alocis was grown in vitro and cigarette smoke extract-responsive genes determined by RNAseq. Mice were exposed, or not, to mainstream 1R6F research cigarette smoke and infected with F. alocis, or not, in an acute ligature model of periodontitis. Key clinical, infectious, and immune data were collected.ResultsIn culture, F. alocis growth was unaffected by smoke conditioning and only a small number of genes were specifically regulated by smoke exposure. Reduced murine mass, differences in F. alocis-cognizant antibody production, and altered immune profiles as well as altered alveolar bone loss were all attributable to smoke exposure and/or F. alocis infection in vivo.ConclusionsF. alocis is well-adapted to tobacco-rich conditions and its pathogenesis is enhanced by tobacco smoke exposure. A smoke-exposed ligature model of periodontitis shows promise as a tool with which to further unravel mechanisms underlying tobacco-enhanced, bacteria-induced disease.
| S-EPMC9976951 | biostudies-literature