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Lookup NU author(s): Dr Min Yu
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0).
Periodontal disease (PD) is characterized by continuous leukocyte infiltration. CCL2 plays an important role in periodontal pathogenesis. In this study, we studied the possibility of a pathway involved in the production of CCL2 in peripheral blood (PB) and gingival tissues of chronic periodontitis (CP) and aggressive periodontitis (AgP) patients based on our previous work about chemokine signaling pathway leading to production of CCL2 in rheumatoid arthritis (RA) patients. Total RNA was isolated from PB leukocytes and gingival tissue in periodontitis patients and healthy controls. Real-time PCR was used to determine CCL4, CCR5, NF-κB, and CCL2 expression. Serum level of CCL2 was assessed by enzyme-linked immunosorbent assay. The production of CCL2 in gingival tissue was analyzed by immunohistochemistry. The expression of CCL2 mRNA in CP and AgP patients was greatly decreased than those in healthy controls, both in gingival tissue and on PB leukocyte. The mRNA expression levels of CCL4, CCR5 and NF-κB in the patients with different periodontal diseases were higher than those in the Healthy group. However, in spite of the higher expression of NF-κB on AgP PB leukocytes, and more intense CCR5 expression in the CP gingival tissue, the differences were not statistically significant. Serum CCL2 levels were elevated in both CP and AgP patients. Histological examination of CP patients revealed extensive CCL2 expression in mild inflamed gingival tissue. These data provide evidence that the CCL4/CCR5/NF-κB pathway may be involved in CCL2 expression on PB leukocytes of clinically CP patients.
Author(s): Zhang L, Wang Y, Wang H, Huang Q, Yu M, Bao G, Li C, Deng J, Cui Z, Cao D
Publication type: Article
Publication status: Published
Journal: International Journal of Clinical and Experimental Pathology
Year: 2017
Volume: 10
Issue: 4
Pages: 4400-4410
Print publication date: 15/04/2017
Online publication date: 01/04/2017
Acceptance date: 25/02/2017
Date deposited: 02/06/2017
ISSN (electronic): 1936-2625
Publisher: E-Century Publishing Corporation
URL: http://www.ijcep.com/V10_No4.html