Authors: Taheri, Mohammad | Gholami, Leila | Nicknafs, Fwad | Hussen, Bashdar Mahmud | Arsang-Jang, Shahram | Sayad, Arezou | Ghafouri-Fard, Soudeh
Article Type:
Research Article
Abstract:
Periodontal diseases are common conditions in almost all age groups and a public health problem. Numerous risk factors have been demonstrated for this condition. The main mechanism of tissue destruction in the periodontitis is the functional interactions between microbial pathogens and host immune responses, thus cytokines have crucial roles in the pathogenesis periodontitis. Our previous study has demonstrated the susceptibility role of HLA-DRB1*04 allele in development of this disease. So, the individuals who were positive for HLA-DRB1*04 allele were excluded. We aimed to appraise the function of cytokines in the pathogenesis of periodontitis via assessment of tissue and blood levels
…of a number of cytokine coding genes, namely IL-1B , CXCL8 , IL-17 , IFNG , TGFB and TNFA1 . Expressions of IFNG , IL-17 , TGFB and TNFA1 were significantly higher in the peripheral blood of individuals with periodontitis compared with unaffected persons (Posterior beta = 1.91, P value = 0.043; Posterior beta = 1.84, P value = 0.033; Posterior beta = 0.713, P value = 0.009 and Posterior beta = 2.85, P value = 0.001, respectively). Moreover, expression of IL-17 was higher in females compared with males (Posterior beta = 1.47, P value = 0.036). As the interaction effect between gender and group was remarkable for IL-17 expression, we further conducted subgroup analysis within gender group. Expression of IL-17 was higher in male patients compared with unaffected males (Posterior beta = 1.9, P value = 0.048). We did not detect any significant difference in the expression of these cytokines in tissues obtained from affected individuals and unaffected controls. Therefore, our results imply dysregulation of cytokine coding genes in patients with periodontitis and warrant further mechanistical studies.
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Keywords: Periodontitis, cytokine, IFNG, IL-17, TGFB, TNFA1
DOI: 10.3233/HAB-211507
Citation: Human Antibodies,
vol. 30, no. 1, pp. 47-55, 2022
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