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Porphyromonas gingivalis Facilitates the Development and Progression of Destructive Arthritis through Its Unique Bacterial Peptidylarginine Deiminase (PAD)
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نویسنده
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maresz k.j. ,hellvard a. ,sroka a. ,adamowicz k. ,bielecka e. ,koziel j. ,gawron k. ,mizgalska d. ,marcinska k.a. ,benedyk m. ,pyrc k. ,quirke a.-m. ,jonsson r. ,alzabin s. ,venables p.j. ,nguyen k.-a. ,mydel p. ,potempa j.
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منبع
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plos pathogens - 2013 - دوره : 9 - شماره : 9
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چکیده
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Rheumatoid arthritis and periodontitis are two prevalent chronic inflammatory diseases in humans and are associated with each other both clinically and epidemiologically. recent findings suggest a causative link between periodontal infection and rheumatoid arthritis via bacteria-dependent induction of a pathogenic autoimmune response to citrullinated epitopes. here we showed that infection with viable periodontal pathogen porphyromonas gingivalis strain w83 exacerbated collagen-induced arthritis (cia) in a mouse model,as manifested by earlier onset,accelerated progression and enhanced severity of the disease,including significantly increased bone and cartilage destruction. the ability of p. gingivalis to augment cia was dependent on the expression of a unique p. gingivalis peptidylarginine deiminase (ppad),which converts arginine residues in proteins to citrulline. infection with wild type p. gingivalis was responsible for significantly increased levels of autoantibodies to collagen type ii and citrullinated epitopes as a ppad-null mutant did not elicit similar host response. high level of citrullinated proteins was also detected at the site of infection with wild-type p. gingivalis. together,these results suggest bacterial pad as the mechanistic link between p. gingivalis periodontal infection and rheumatoid arthritis. © 2013 maresz et al.
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آدرس
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department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, broegelmann research laboratory,department of clinical science,university of bergen,bergen,norway,department of rheumatology and inflammation research,sahlgrenska academy,university of gothenburg,gothenburg, Sweden, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of human developmental biology,jagiellonian university college of medicine,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow, Poland, kennedy institute of rheumatology,university of oxford,london, United Kingdom, broegelmann research laboratory,department of clinical science,university of bergen,bergen, Norway, kennedy institute of rheumatology,university of oxford,london, United Kingdom, kennedy institute of rheumatology,university of oxford,london, United Kingdom, institute of dental research,westmead centre for oral health and westmead millennium institute,sydney,australia,department of oral biology,university of sydney,sydney, Australia, broegelmann research laboratory,department of clinical science,university of bergen,bergen,norway,department of rheumatology and inflammation research,sahlgrenska academy,university of gothenburg,gothenburg, Sweden, department of microbiology,biophysics and biotechnology,jagiellonian university,krakow,poland,university of louisville school of dentistry,center for oral health and systemic diseases,louisville,ky, United States
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Authors
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