Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-63939
Belibasakis, Georgios N; Guggenheim, Bernhard; Bostanci, Nagihan (2013). Down-regulation of NLRP3 inflammasome in gingival fibroblasts by subgingival biofilms: Involvement of Porphyromonas gingivalis. Innate Immunity, 19(1):3-9.
Recognition of pathogen-associated molecular patterns that activate IL-1β is regulated by inflammasomes, predominantly of the nucleotide-binding oligomerization domain-like receptor (NLR) family. NLRP3 inflammasome is involved in the innate immune responses in periodontal disease. This is an inflammatory condition that destroys the tooth-supporting (periodontal) tissues, initiated by the subgingival formation of multi-species biofilms, frequently including the Gram-negative species Porphyromonas gingivalis. The aim of this study was to investigate the relative effect of P. gingivalis as part of subgingival biofilm, on the expressions of NLRP3 inflammasome, absent in melanoma (AIM)2 (a non-NLR inflammsome) and IL-1β by human gingival fibroblasts. The 10-species subgingival biofilm model, or its 9-species variant excluding P. gingivalis, were used to challenge the cells for 6 h. Gene expression analysis for various inflammasome components and IL-1β was performed by TaqMan real-time PCR. The 10-species subgingival biofilm reduced NLRP3 and IL-1β, but did not affect AIM2 expression. Exclusion of P. gingivalis from the biofilm partially rescued NLRP3 and IL-1β expressions. In conclusion, subgingival biofilms down-regulate NLRP3 and IL-1β expression, partly because of P. gingivalis. These dampened host innate immune responses may favour the survival and persistence of the associated biofilm species in the periodontal tissues.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Center for Dental Medicine > Institute of Oral Biology|
|DDC:||610 Medicine & health|
|Deposited On:||31 Jul 2012 13:48|
|Last Modified:||03 Dec 2013 02:25|
|Citations:||Web of Science®. Times cited: 1|
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