Chemokines and cytokines profile in whole saliva of patients with periodontitis

趋化因子 唾液 牙周炎 促炎细胞因子 免疫学 免疫系统 医学 内科学 炎症
作者
Dione Kawamoto,Pâmela Pontes Penas Amado,Emmanuel Albuquerque‐Souza,Manuela Rocha Bueno,Gláuber Campos Vale,Luciana Saraiva,Márcia Pinto Alves Mayer
出处
期刊:Cytokine [Elsevier]
卷期号:135: 155197-155197 被引量:30
标识
DOI:10.1016/j.cyto.2020.155197
摘要

Clinical features suggest differences in immune response among periodontitis forms, albeit a large number of cytokines and chemokines remain to be evaluated. The saliva is an available source of mediators and its analysis would be valuable in order to understand pathophysiological differences. The objective of this study was analyze chemokines/cytokines profile in whole saliva of individuals with severe periodontitis (Stage III) presenting moderate [Grade B; GB] or rapid progression rate with a localized incisor-molar pattern [Grade C; GC/IMP]. A case-control study was designed for each periodontitis group. GB (n = 9) and GC/IMP (n = 7) patients and their healthy controls (C-GB, n = 9 and C-GC, n = 7) were evaluated. Non-stimulated saliva samples were assessed by a multiplex assay for a total of 40 cytokines, C-C and C-X-C motif chemokines. GC/IMP group presented higher levels of CCL17 and CCL27 (p = 0.04, FDR > 0.05), and lower levels of CCL2 (p = 0.04, FDR > 0.05) and CCL25 (p = 0.006, FDR < 0.05) when compared to its control. GB patients had higher levels of IL-6, IL-1β (p = 0.04, FDR > 0.05), and elevated pro-inflammatory (TNF-α,IL-1β,INF-γ,IL-6, IL-16): anti-inflammatory (IL-2, IL-4, IL-10) ratio (p = 0.01, FDR < 0.05) compared to its control [p-values by Mann-Whitney test, and False Discovery Rate (FDR) by Benjamini-Hochburg corrections]. CCL-chemokines and cytokines contributed to differences between GC/C-GC and GB/C-GB, respectively (p < 0.05, PERMANOVA test). These preliminary data revealed that each periodontitis phenotype presented distinct immune profiles differentially expressed in saliva compared to their related controls, suggesting differences in the etiopathogenesis of GB and GC/IMP.
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