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(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

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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
[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

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