Interferon-γ, interleukins-6 and -4, and factor XIII-A as indirect markers of the classical and alternative macrophage activation pathways in chronic periodontitis.
BACKGROUND
Macrophages account for 5% to 30% of the inflammatory infiltrate in periodontitis and are activated by the classic and alternative pathways. These pathways are identified by indirect markers, among which interferon (IFN)-γ and interleukin-6 (IL)-6 of the classic pathway and IL-4 of the alternative pathway have been studied widely. Recently, factor XIII-A (FXIII-A) was reported to be a good marker of alternative pathway activation. The aim of this study is to determine the macrophage activation pathways involved in chronic periodontitis (CP) by the detection of the indirect markers IFN-γ, IL-6, FXIII-A, and IL-4.


METHODS
Biopsies were taken from patients with CP (n = 10) and healthy individuals (n = 10) for analysis of IFN-γ, IL-6, IL-4, and FXIII-A by Western blot (WB), immunohistochemistry (IHC), and enzyme-linked immunosorbent assay (ELISA). The same biopsies of healthy and diseased gingival tissue were used, and the expressions of these markers were compared between healthy individuals and those with CP.


RESULTS
The presence of macrophages was detected by CD68+ immunohistochemistry and their IFN-γ, IL-6, IL-4, and FXIII-A markers by WB, IHC, and ELISA in all samples of healthy and diseased tissue. IL-6, IL-4, and FXIII-A were significantly higher in patients with CP, whereas FXIII-A was higher in healthy individuals.


CONCLUSIONS
The presence of IFN-γ, IL-6, IL-4, and FXIII-A in healthy individuals and in patients with CP suggests that macrophages may be activated by both classic and alternative pathways in health and in periodontal disease.
Department of Conservative Dentistry, Faculty of Dentistry, University Andrés Bello, Viña del Mar, Chile.
Mariely
M
Navarrete
Jocelyn
J
García
Nicolás
N
Dutzan
Leslie
L
Henríquez
Javier
J
Puente
Paola
P
Carvajal
Marcela
M
Hernandez
Jorge
J
Gamonal
D000199:Actins / Q000032:analysis; D000328:Adult; D016301:Alveolar Bone Loss / Q000276:immunology; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D001706:Biopsy; D015153:Blotting, Western; D055113:Chronic Periodontitis / Q000276:immunology*; D003774:Dental Plaque Index; D004797:Enzyme-Linked Immunosorbent Assay; D026122:Factor XIIIa / Q000032:analysis*; D005260:Female; D005881:Gingiva / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000032:analysis*; D015847:Interleukin-4 / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis*; D008262:Macrophage Activation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000276:immunology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000276:immunology; D000097382:CD68 Molecule
D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D026122:Factor XIIIa; D007371:Interferon-gamma; D015847:Interleukin-4; D015850:Interleukin-6; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C508598:IL4 protein, human; C508600:IL6 protein, human