Interleukin Gene Variability and Periodontal Bacteria in Patients with Generalized Aggressive Form of Periodontitis

Abstract

<jats:p>Host genetic predispositions to dysregulated immune response can influence the development of the aggressive form of periodontitis (AgP) through susceptibility to oral dysbiosis and subsequent host-microbe interaction. This case-control study aimed to perform a multilocus analysis of functional variants in selected interleukin (IL) genes in patients with the generalized form of AgP in a homogenous population. Twelve polymorphisms in IL-1 gene cluster, IL-6 and its receptor, IL-10, IL-17A, and IL-18 were determined in 91 AgP patients and 210 controls. Analysis of seven selected periodontal bacteria in subgingival sulci/pockets was performed with a commercial DNA-microarray kit in a subgroup of 76 individuals. The pilot in vitro study included stimulation of peripheral blood monocytes (PBMC) from 20 individuals with periodontal bacteria and measurement of IL-10 levels using the Luminex method. Only the unctional polymorphism IL-10 −1087 A/G (rs1800896) and specific IL-10 haplotypes were associated with the development of the disease (p &lt; 0.05, Pcorr &gt; 0.05). Four bacterial species occurred more frequently in AgP than in controls (p &lt; 0.01, Pcorr &lt; 0.05). Elevated IL-10 levels were found in AgP patients, carriers of IL-10 −1087GG genotype, and PBMCs stimulated by periodontal bacteria (p &lt; 0.05, Pcorr &gt; 0.05). We therefore conclude that a combination of genetic predisposition to the altered expression of IL-10 and the presence of specific periodontal bacteria may contribute to Th1/Th2 balance disruption and AgP development.</jats:p>

IL-18 Gene rs187238 and rs1946518 Polymorphisms and Expression in Gingival Tissue in Patients with Periodontitis

“…The results in Noack et al [ 21 , 22 ] also suggest lack of association between IL-18 gene polymorphism and periodontal disease in the German population. Similarly, in the studies by Vokurka et al [ 23 ] and Borilova Linhartova et al [ 24 ], there was no statistically significant association between IL-18 gene polymorphism and periodontal disease in a Czech population. Martelli et al [ 25 ] found a moderate association between IL-18 gene polymorphisms and chronic and aggressive periodontal disease in an Italian population.…”

Innate and adaptive immunity of periodontal disease. From etiology to alveolar bone loss

“…Under normal conditions, this subgingival environment is rich in immune and inflammatory mediators, which imposes a challenge on the survival of pathogenic bacteria. However, when the host's immune response is dysregulated due to changes in the microbial community or due to immune‐regulatory defects, it is difficult to restrict bacterial growth, thus manifesting the pathogenicity (Borilova Linhartova et al., 2020).…”

Cytokines and Their Genetic Polymorphisms Related to Periodontal Disease

“…The authors of another study have shown that P. gingivalis, in patients with chronic periodontitis, induces the production of IL-6, which was significantly increased in carriers of the IL-6 gene −174G allele [ 161 ]. Borilova Linhartova et al examined the associations between IL-1, IL-6, IL-10, IL-17A, and IL-18 gene polymorphisms and the bacterial colonisation in patients with aggressive periodontitis [ 162 ]. The authors found that patients with the IL-10 −1087GG genotype have increased IL-10 plasma levels, as well as IL-10 expression in peripheral blood monocytes stimulated in vitro by periodontal bacteria [ 162 ].…”

“…Borilova Linhartova et al examined the associations between IL-1, IL-6, IL-10, IL-17A, and IL-18 gene polymorphisms and the bacterial colonisation in patients with aggressive periodontitis [ 162 ]. The authors found that patients with the IL-10 −1087GG genotype have increased IL-10 plasma levels, as well as IL-10 expression in peripheral blood monocytes stimulated in vitro by periodontal bacteria [ 162 ]. In another study, these authors indicated that the release of IL-17 by mononuclear cells stimulated by periodontal bacteria was increased in carriers of the IL-17A −197A allele [ 163 ].…”