Advanced search
Start date
Betweenand
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

NLRC4 inflammasome has a protective role on inflammatory bone resorption in a murine model of periodontal disease

Full text
Author(s):
Rocha, Fernanda R. G. [1, 2] ; Delitto, Andrea E. [3] ; Chaves de Souza, Joao A. [4] ; Maldonado, Laura A. G. [2] ; Wallet, Shannon M. [5] ; Rossa Jr, Carlos
Total Authors: 6
Affiliation:
[1] Univ Florida, Coll Dent, Dept Oral Biol, Gainesville, FL 32610 - USA
[2] UNESP State Univ Sao Paulo, Sch Dent Araraquara, Dept Diag & Surg, Araraquara, SP - Brazil
[3] Univ Florida, Hlth Sci Ctr, Dept Phys Therapy, Gainesville, FL - USA
[4] Fed Univ Goias UFG, Sch Dent, Dept Stomatol, Goiania, Go - Brazil
[5] East Carolina Univ, Coll Dent Med, Dept Foundat Sci, Greenville, NC 27858 - USA
Total Affiliations: 5
Document type: Journal article
Source: Immunobiology; v. 225, n. 1 JAN 2020.
Web of Science Citations: 0
Abstract

There is virtually no information on the role of NLRC4 inflammasome on bone resorption and inflammation associated with periodontitis. Bacterial-associated experimental periodontitis was induced in wild-type (WT) and Nlrc4-KO C57BL/6 mice. 3 mu L of a 1 x 10(9) UFC/mL PBS suspension of heat-killed Gram-negative bacteria were injected (3x/week for 4 weeks) directly into the gingival tissues of WT and Nlrc4-KO mice (n = 6/genotype). Control animals were injected bilaterally (3x/week for 4 weeks) in the same sites with the same volume of the PBS vehicle. Alveolar bone resorption was quantified by mu CT. Inflammatory infiltrate in the gingival tissues was assessed qualitatively in H\&E-stained slides and by the detection of a pan-leukocyte marker (CD45) and a neutrophil marker (Ly6G) using immunofluorescence. Modulation of Rankl, Mmp-13, Tnf-a, Il-6 and Il-10 expression in the gingival tissues was determined by RT-qPCR. Osteoclastogenesis was assessed in vivo by biochemical staining for TRAP. The relevance of NLRC4 for RANKL-induced osteoclastic differentiation and activity was investigated in vitro using bone marrow-derived macrophages from WT and Nlrc4-KO mice. Bone resorption was significantly greater in Nlrc4-KO mice; however there were no differences between WT and Nlrc4-KO mice on osteoclast numbers and on the inflammatory infiltrate. In vitro, osteoclast activity was significantly enhanced in Nlrc4-deficient macrophages; whereas RANKL-induced differentiation was not affected. Expression of the selected candidate genes was also similarly increased by the induction of experimental periodontal disease, except for the expression of Tnf-alpha and Il-10, which was already significantly higher in the gingival tissues of Nlrc4-KO mice. We conclude that NLRC4 inflammasome has a protective role on inflammatory bone resorption in this experimental model. Furthermore, the bone-sparing effect may be related with the modulation of osteoclast activity. (AU)

FAPESP's process: 14/17544-6 - NLRC4 inflammasome and the immune response and bone resorption in experimental periodontal disease
Grantee:Fernanda Regina Godoy Rocha
Support type: Scholarships abroad - Research Internship - Doctorate
FAPESP's process: 14/04926-8 - NLRC4 and NLRP3 inflammasomes in experimental periodontal disease induced by Aggregatibacter actinomycetemcomitans
Grantee:Fernanda Regina Godoy Rocha
Support type: Scholarships in Brazil - Doctorate