scholarly journals Association of the rgpB gingipain genotype to the major fimbriae (fimA) genotype in clinical isolates of the periodontal pathogen Porphyromonas gingivalis

2015 ◽  
Vol 7 (1) ◽  
pp. 29124 ◽  
Author(s):  
Anne Karin Kristoffersen ◽  
Silje J. Solli ◽  
Toan Duy Nguyen ◽  
Morten Enersen
Keyword(s):  
Porphyromonas Gingivalis ◽  
Clinical Isolates ◽  
Periodontal Pathogen ◽  
Fima Genotype

scholarly journals Existence of natural mouse IgG mAbs recognising epitopes shared by malondialdehyde acetaldehyde adducts and Porphyromonas gingivalis

2021 ◽  
Vol 27 (2) ◽  
pp. 158-169
Author(s):  
Mikael Kyrklund ◽  
Heidi Kaski ◽  
Ramin Akhi ◽  
Antti E Nissinen ◽  
Outi Kummu ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Low Density Lipoprotein ◽  
Physiological Role ◽  
Density Lipoprotein ◽  
Tissue Homeostasis ◽  
Innate Immune ◽  
Periodontal Pathogen ◽  
First Line ◽  
Germline Genes ◽  
Innate Recognition

Natural Abs are produced by B lymphocytes in the absence of external Ag stimulation. They recognise self, altered self and foreign Ags, comprising an important first-line defence against invading pathogens and serving as innate recognition receptors for tissue homeostasis. Natural IgG Abs have been found in newborns and uninfected individuals. Yet, their physiological role remains unclear. Previously, no natural IgG Abs to oxidation-specific epitopes have been reported. Here, we show the cloning and characterisation of mouse IgG mAbs against malondialdehyde acetaldehyde (MAA)-modified low-density lipoprotein. Sequence analysis reveals high homology with germline genes, suggesting that they are natural. Further investigation shows that the MAA-specific natural IgG Abs cross-react with the major periodontal pathogen Porphyromonas gingivalis and recognise its principle virulence factors gingipain Kgp and long fimbriae. The study provides evidence that natural IgGs may play an important role in innate immune defence and in regulation of tissue homeostasis by recognising and removing invading pathogens and/or modified self-Ags, thus being involved in the development of periodontitis and atherosclerosis.

scholarly journals Modulation of an Interleukin-12 and Gamma Interferon Synergistic Feedback Regulatory Cycle of T-Cell and Monocyte Cocultures by Porphyromonas gingivalis Lipopolysaccharide in the Absence or Presence of Cysteine Proteinases

2002 ◽  
Vol 70 (10) ◽  
pp. 5695-5705 ◽  
Author(s):  
Peter L. W. Yun ◽  
Arthur A. DeCarlo ◽  
Charles Collyer ◽  
Neil Hunter
Keyword(s):  
T Cells ◽  
T Cell ◽  
Porphyromonas Gingivalis ◽  
Gamma Interferon ◽  
Periodontal Pathogen ◽  
Interleukin 12 ◽  
Minor Role ◽  
Cysteine Proteinases ◽  
Activated T Cells ◽  
Ifn Γ

ABSTRACT Interleukin 12 (IL-12) is an efficient inducer and enhancer of gamma interferon (IFN-γ) production by both resting and activated T cells. There is evidence that human monocytes exposed to IFN-γ have enhanced ability to produce IL-12 when stimulated with lipopolysaccharide (LPS). In this study, it was demonstrated that LPS from the oral periodontal pathogen Porphyromonas gingivalis stimulated monocytes primed with IFN-γ to release IL-12, thereby enhancing IFN-γ accumulation in T-cell populations. P. gingivalis LPS was shown to enhance IL-12 induction of IFN-γ in T cells in a manner independent from TNF-α contribution. The levels of T-cell IL-12 receptors were not affected by P. gingivalis LPS and played only a minor role in the magnitude of the IFN-γ response. These data suggest that LPS from P. gingivalis establishes an activation loop with IL-12 and IFN-γ with potential to augment the production of inflammatory cytokines in relation to the immunopathology of periodontitis. We previously reported that the major cysteine proteinases (gingipains) copurifying with LPS in this organism were responsible for reduced IFN-γ accumulation in the presence of IL-12. However, the addition of the gingipains in the presence of LPS resulted in partial restoration of the IFN-γ levels. In the destructive periodontitis lesion, release of gingipains from the outer membrane (OM) of P. gingivalis could lead to the downregulation of Th1 responses, while gingipain associated with LPS in the OM or in OM vesicles released from the organism could have net stimulatory effects.

scholarly journals Retraction Note: Temporal activation of anti- and pro-apoptotic factors in human gingival fibroblasts infected with the periodontal pathogen, Porphyromonas gingivalis: potential role of bacterial proteases in host signalling

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Sonya Urnowey ◽  
Toshihiro Ansai ◽  
Vira Bitko ◽  
Koji Nakayama ◽  
Tadamichi Takehara ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Potential Role ◽  
Human Gingival Fibroblasts ◽  
Periodontal Pathogen ◽  
Gingival Fibroblasts ◽  
The University ◽  
Apoptotic Factors

The Editor has retracted this article [1] following an investigation by the University of South Alabama which found:

scholarly journals Potential Role of Phosphoglycerol Dihydroceramide Produced by Periodontal Pathogen Porphyromonas gingivalis in the Pathogenesis of Alzheimer’s Disease

2020 ◽  
Vol 11 ◽  
Author(s):  
Chiaki Yamada ◽  
Juliet Akkaoui ◽  
Anny Ho ◽  
Carolina Duarte ◽  
Richard Deth ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Porphyromonas Gingivalis ◽  
Virulence Factors ◽  
Potential Role ◽  
Sirtuin 1 ◽  
Periodontal Pathogen ◽  
Secretory Phenotype ◽  
Aβ42 Peptide

BackgroundAmong different types of sphingolipids produced by human cells, the possible engagement of ceramide species in the pathogenesis of Alzheimer’s disease (AD) has attracted recent attention. While ceramides are primarily generated by de novo synthesis in mammalian cells, only a limited number of bacterial species, produce ceramides, including phosphoglycerol dihydroceramide (PGDHC) that is produced by the key periodontal pathogen Porphyromonas gingivalis. Emerging evidence indicates that virulence factors produced by P. gingivalis, such as lipopolysaccharide and gingipain, may be engaged in the initiation and/or progression of AD. However, the potential role of PGDHC in the pathogenesis of AD remains unknown. Therefore, the aim of this study was to evaluate the influence of PGDHC on hallmark findings in AD.Material and MethodsCHO-7WD10 and SH-SY-5Y cells were exposed to PGDHC and lipopolysaccharide (LPS) isolated from P. gingivalis. Soluble Aβ42 peptide, amyloid precursor protein (APP), phosphorylated tau and senescence-associated secretory phenotype (SASP) factors were quantified using ELISA and Western blot assays. ResultsOur results indicate that P. gingivalis (Pg)-derived PGDHC, but not Pg-LPS, upregulated secretion of soluble Aβ42 peptide and expression of APP in CHO-7WD10 cells. Furthermore, hyperphosphorylation of tau protein was observed in SH-SY-5Y cells in response to PGDHC lipid. In contrast, Pg-LPS had little, or no significant effect on the tau phosphorylation induced in SH-SY-5Y cells. However, both PGDHC and Pg-LPS contributed to the senescence of SH-SY5Y cells as indicated by the production of senescence-associated secretory phenotype (SASP) markers, including beta-galactosidase, cathepsin B (CtsB), and pro-inflammatory cytokines TNF-α, and IL-6. Additionally, PGDHC diminished expression of the senescence-protection marker sirtuin-1 in SH-SY-5Y cells.ConclusionsAltogether, our results indicate that P. gingivalis-derived PGDHC ceramide promotes amyloidogenesis and hyperphosphorylation, as well as the production of SASP factors. Thus, PGDHC may represent a novel class of bacterial-derived virulence factors for AD associated with periodontitis.

scholarly journals Molecular Mechanism for Connective Tissue Destruction by Dipeptidyl Aminopeptidase IV Produced by the Periodontal Pathogen Porphyromonas gingivalis

2005 ◽  
Vol 73 (5) ◽  
pp. 2655-2664 ◽  
Author(s):  
Yumi Kumagai ◽  
Hisao Yagishita ◽  
Ayako Yajima ◽  
Tatsuya Okamoto ◽  
Kiyoshi Konishi
Keyword(s):  
Connective Tissue ◽  
Molecular Mechanism ◽  
Porphyromonas Gingivalis ◽  
Type I Collagen ◽  
Plasmid Vector ◽  
Periodontal Pathogen ◽  
Matrix Metalloproteinase 2 ◽  
Type I ◽  
Tissue Destruction ◽  
Dipeptidyl Aminopeptidase

ABSTRACT Porphyromonas gingivalis is a pathogen associated with adult periodontitis. It produces dipeptidyl aminopeptidase IV (DPPIV), which may act as a virulence factor by contributing to the degradation of connective tissue. We investigated the molecular mechanism by which DPPIV contributes to the destruction of connective tissue. DPPIV itself did not show gelatinase or collagenase activity toward human type I collagen, but it promoted the activity of the host-derived matrix metalloproteinase 2 (MMP-2) (gelatinase) and MMP-1 (collagenase). DPPIV bound to fibronectin and mediated the adhesion of P. gingivalis to fibronectin. Mutant DPPIV with catalytic Ser mutagenized to Ala (DPPSA) did not accelerate the degradation of collagen and gelatin by MMPs but retained fibronectin-binding activity. The adhesion of human gingival fibroblasts and NIH 3T3 cells to fibronectin was inhibited by DPPIV. Strain 4351ADPPSA exhibited an intermediate level of virulence in mice, between that of the strain expressing wild-type DPPIV (4351ADPP) and that of the strain harboring only the plasmid vector (4351AVEC). It is suggested that both activity promoting the degradation of collagen and gelatin and binding to fibronectin are required for full virulence. These results reveal novel biological functions of DPPIV and suggest a pathological role in the progression of periodontitis.

scholarly journals Porphyromonas gingivalis Ferrous Iron Transporter FeoB1 Influences Sensitivity to Oxidative Stress

2009 ◽  
Vol 78 (2) ◽  
pp. 688-696 ◽  
Author(s):  
Cecilia Anaya-Bergman ◽  
Jia He ◽  
Kevin Jones ◽  
Hiroshi Miyazaki ◽  
Andrew Yeudall ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mutant Strain ◽  
Porphyromonas Gingivalis ◽  
Ferrous Iron ◽  
Atmospheric Oxygen ◽  
Host Cells ◽  
Periodontal Pathogen ◽  
Bacterial Survival ◽  
Deficient Mutant ◽  
Iron Transporter

ABSTRACT Porphyromonas gingivalis FeoB1 is a ferrous iron transporter. Analysis of parental and feoB1-deficient strains of the periodontal pathogen revealed that the feoB1-deficient mutant strain had an increased ability to survive oxidative stress. Specifically, survival of the mutant strain was increased 33% with exposure to peroxide and 5% with exposure to atmospheric oxygen compared to the parental strain. Interestingly, the ability to survive intracellularly also increased fivefold in the case of the feoB1-deficient mutant. Our data suggest that although the FeoB1 protein is required for ferrous iron acquisition in P. gingivalis, it also has an adverse effect on survival of the bacterium under oxidative stress conditions. Finally, we show that feoB1 expression is not iron dependent and is dramatically reduced in the presence of host cells, consistent with the observed deleterious role it plays in bacterial survival.

scholarly journals Cell Cycle Arrest and Apoptosis Induced by Porphyromonas gingivalis Require Jun N-Terminal Protein Kinase- and p53-Mediated p38 Activation in Human Trophoblasts

2018 ◽  
Vol 86 (4) ◽  
Author(s):  
Hiroaki Inaba ◽  
Atsuo Amano ◽  
Richard J. Lamont ◽  
Yukitaka Murakami ◽  
Michiyo Matsumoto-Nakano
Keyword(s):  
Protein Kinase ◽  
Signaling Pathways ◽  
Porphyromonas Gingivalis ◽  
Cellular Damage ◽  
Periodontal Pathogen ◽  
Extravillous Trophoblast ◽  
Low Birth Weight Infants ◽  
Terminal Protein ◽  
Content Type ◽  
Cellular Dna

ABSTRACT Porphyromonas gingivalis , a periodontal pathogen, has been implicated as a causative agent of preterm delivery of low-birth-weight infants. We previously reported that P. gingivalis activated cellular DNA damage signaling pathways and ERK1/2 that lead to G 1 arrest and apoptosis in extravillous trophoblast cells (HTR-8 cells) derived from the human placenta. In the present study, we further examined alternative signaling pathways mediating cellular damage caused by P. gingivalis. P. gingivalis infection of HTR-8 cells induced phosphorylation of p38 and Jun N-terminal protein kinase (JNK), while their inhibitors diminished both G 1 arrest and apoptosis. In addition, heat shock protein 27 (HSP27) was phosphorylated through both p38 and JNK, and knockdown of HSP27 with small interfering RNA (siRNA) prevented both G 1 arrest and apoptosis. Furthermore, regulation of G 1 arrest and apoptosis was associated with p21 expression. HTR-8 cells infected with P. gingivalis exhibited upregulation of p21, which was regulated by p53 and HSP27. These results suggest that P. gingivalis induces G 1 arrest and apoptosis via novel molecular pathways that involve p38 and JNK with its downstream effectors in human trophoblasts.

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