Impacts of Porphyromonas gingivalis periodontitis on rheumatoid arthritis autoimmunity.
Autor: | Ahmadi P; Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran., Mahmoudi M; Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran., Kheder RK; Medical Laboratory Science Department, College of Science, University of Raparin, Rania, Sulaymaniyah, Iraq; Department of Medical Analysis, Faculty of Applied Science, Tishk International University, Erbil, Iraq., Faraj TA; Department of Medical Analysis, Faculty of Applied Science, Tishk International University, Erbil, Iraq; Department of Basic Sciences, College of Medicine, Hawler Medical University, Erbil, Iraq., Mollazadeh S; Natural Products and Medicinal Plants Research center north Khorasan University of Medical Sciences, Bojnurd, Iran., Abdulabbas HS; Continuous Education Department, Faculty of Dentistry, University of Al-Ameed, Karbala 56001, Iraq., Esmaeili SA; Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: esmaeiliar@mums.ac.ir. |
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Jazyk: | angličtina |
Zdroj: | International immunopharmacology [Int Immunopharmacol] 2023 May; Vol. 118, pp. 109936. Date of Electronic Publication: 2023 Mar 14. |
DOI: | 10.1016/j.intimp.2023.109936 |
Abstrakt: | In RA patients' synovial sites, citrullinated RA-related antigens such as type II collagens, fibrin (ogen), vimentin, and α-enolase could be targeted by ACCPAs. Since ACCPA production can be initiated a long time before RA sign appearance, primary auto-immunization against these citrullinated proteins can be originated from extra-articular sites. It has been shown that there is a significant association between P. gingivalis periodontitis, anti- P. gingivalis antibodies, and RA. P. gingivalis gingipains (Rgp, Kgp) can degrade proteins such as fibrin and α-enolase into some peptides in the form of Arg in the C-terminal which is converted to citrulline by PPAD. Also, PPAD can citrullinate type II collagen and vimentins (SA antigen). P. gingivalis induces inflammation and chemoattraction of immune cells such as neutrophils and macrophages through the increase of C5a (gingipain C5 convertase-like activity) and SCFA secretion. Besides, this microorganism stimulates anoikis, a special type of apoptosis, and NETosis, an antimicrobial form of neutrophil death, leading to the release of PAD1-4, α-enolase, and vimentin from apoptotic cells into the periodontal site. In addition, gingipains can degrade macrophages CD14 and decrease their ability in apoptotic cell removal. Gingipains also can cleave IgGs in the Fc region and transform them into rheumatoid factor (RF) antigens. In the present study, the effects of P. gingivalis on rheumatoid arthritis autoimmune response have been reviewed, which could attract practical insight both in bench and clinic. Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2023 Elsevier B.V. All rights reserved.) |
Databáze: | MEDLINE |
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