Expression and regulation of the NALP3 inflammasome complex in periodontal diseases

Summary Periodontitis is an infectious process characterized by inflammation affecting the supporting structures of the teeth. Porphyromonas gingivalis is a major oral bacterial species implicated in the pathogenesis of periodontitis. Processing of interleukin (IL)‐1 family cytokines is regulated by...

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Vydáno v:	Clinical and experimental immunology Ročník 157; číslo 3; s. 415 - 422
Hlavní autoři:	Bostanci, N., Emingil, G., Saygan, B., Turkoglu, O., Atilla, G., Curtis, M. A., Belibasakis, G. N.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Oxford, UK Blackwell Publishing Ltd 01.09.2009 Blackwell Blackwell Science Inc
Témata:	Adult analysis Analysis of Variance Analytical, structural and metabolic biochemistry Apoptosis ASC Biological and medical sciences CARD Signaling Adaptor Proteins Carrier Proteins Carrier Proteins - genetics Case-Control Studies Cell Line Chronic Periodontitis Chronic Periodontitis - immunology Chronic Periodontitis - metabolism Cytoskeletal Proteins Cytoskeletal Proteins - genetics Data processing Facial bones, jaws, teeth, parodontium: diseases, semeiology Female Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation genetics Gingiva Gingiva - immunology Gingiva - metabolism Gingiva - microbiology Gingivitis Humans Immune response immunology Inflammation Inflammatory diseases Interleukin 1 Interleukin 18 Interleukin-18 - genetics Interleukin-1beta Interleukin-1beta - genetics interleukin‐1β Male Medical sciences metabolism methods microbiology Middle Aged Monocytes NALP3 NLR Family, Pyrin Domain-Containing 3 Protein NLRP2 Non tumoral diseases Otorhinolaryngology. Stomatology Periodontal diseases Periodontitis physiology Polymerase chain reaction Porphyromonas gingivalis Porphyromonas gingivalis - physiology Pyrin protein Reverse Transcriptase Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger RNA, Messenger - analysis Teeth Translational Studies Young Adult ASC Periodontal disease Regulation(control) interleukin- 1β Periodontitis Stomatology NALP3 Cytokine NLRP2 Interleukin 1β Biochemistry
ISSN:	0009-9104, 1365-2249, 1365-2249
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Shrnutí:	Summary Periodontitis is an infectious process characterized by inflammation affecting the supporting structures of the teeth. Porphyromonas gingivalis is a major oral bacterial species implicated in the pathogenesis of periodontitis. Processing of interleukin (IL)‐1 family cytokines is regulated by an intracellular innate immune response system, known as the NALP3 [nacht domain‐, leucine‐rich repeat‐, and pyrin domain (PYD)‐containing protein 3] inflammasome complex. The aim of the present study was to investigate by quantitative real‐time polymerase chain reaction (PCR) the mRNA expression of NALP3, its effector molecule apoptosis associated speck‐like protein (ASC), its putative antagonist NLRP2 (NLR family, PYD‐containing protein 2), IL‐1β and IL‐18 (i) in gingival tissues from patients with gingivitis (n = 10), chronic periodontitis (n = 18), generalized aggressive periodontitis (n = 20), as well as in healthy subjects (n = 20), (ii) in vitro in a human monocytic cell line (Mono‐Mac‐6), in response to P. gingivalis challenge for 6 h. The clinical data indicate that NALP3 and NLRP2, but not ASC, are expressed at significantly higher levels in the three forms of inflammatory periodontal disease compared to health. Furthermore, a positive correlation was revealed between NALP3 and IL‐1β or IL‐18 expression levels in these tissues. The in vitro data demonstrate that P. gingivalis deregulates the NALP3 inflammasome complex in Mono‐Mac‐6 cells by enhancing NALP3 and down‐regulating NLRP2 and ASC expression. In conclusion, this study reveals a role for the NALP3 inflammasome complex in inflammatory periodontal disease, and provides a mechanistic insight to the host immune responses involved in the pathogenesis of the disease by demonstrating the modulation of this cytokine‐signalling pathway by bacterial challenge.
Bibliografie:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0009-9104 1365-2249 1365-2249
DOI:	10.1111/j.1365-2249.2009.03972.x