The mRNA and protein levels of IL-10, IL-1β, and RANKL, as well as mRNA levels of TNF-α, were positively correlated with the number of IL-10 producing CD19<sup>+</sup> B cells, which highlights the importance of these factors in the development and progression of periodontitis.
Visfatin was positively correlated with the levels of NF-κB<sub>1</sub> (r = 0.549, P < 0.05), NF-κB<sub>2</sub> (r = 0.636, P < 0.05), PI3k (r = 0.682, P < 0.01), TNF-α (r = 0.558, P < 0.05), and IL-1β (r = 0.686, P < 0.01) in the tissues with periodontitis.
Denervation effectively aggravates ligature-induced rat periodontitis by the NF-κB signaling pathway for excessive production of IL-1β and TNF-α and increased osteoclasts for decreased OPG/RANKL ratio.
In this longitudinally monitored male population, observed effect of baseline central adiposity on future periodontitis progression is conditional on proinflammatory IL-1 genetic variations.
Macrophages become refractory to further LPS challenge, whereby production of key periodontitis associated cytokines TNF and IL-1β is reduced after exposure to LPS during the polarisation phase, even in the presence of inflammatory polarising cytokines.
Surprisingly, hypoxia reversed the effects of <i>P. gingivalis</i> LPS, highly promoted caspase-1 activation and IL-1β maturation.<i>E. coli</i> LPS, a kind of pathogen-associated molecular pattern (PAMP) was chosen to simulate the effect of Gram-negative microbiota.Different from <i>P. gingivalis</i> LPS, <i>E. coli</i> LPS enhanced IL-1β maturation both in normoxia and hypoxia.Moreover, <i>E. coli</i> LPS turned normoxia into hypoxia phase in experimental periodontitis model, which may subsequently propel the inflammatory effect of <i>P. gingivalis</i> LPS.It was concluded that <i>E. coli</i> LPS induced a hypoxic phase, which is a combing pathological factor of <i>P. gingivalis</i> LPS in caspase-1 activating and IL-1β maturation in periodontal inflammation.
Are selected IL-1 polymorphisms and selected subgingival microorganisms significantly associated to periodontitis in type 2 diabetes patients? a clinical study.
The aim of this study was to determine associations between interleukin (IL)-1A (+4845), IL-1B (+3954), and IL-1 receptor antagonist (RN) variable number tandem repeat polymorphisms and adverse pregnancy outcomes and periodontitis in a Turkish women.
Interleukin-1 (IL-1) is a proinflammatory cytokine that plays an important role in the pathogenesis of periodontitis, and so it might be useful to detect high-risk cases of peri-implantitis.
The aim of this study was to test if polymorphisms of genes of IL-1α(+4845) and IL-1β(+3954) were linked with periodontitis, in a case-control study population, delimited to a specific geographic area, in association with microbiological findings.
Previous studies have indicated that type-1 and type-2 interleukin-1 (IL-1) receptors (IL-1R1 and IL-1R2) play important roles in periodontitis progression.
We first examined destruction of periodontal connective tissues in adult PTPα(+/+) and PTPα(-/-) mice subjected to ligature-induced periodontitis, which increases the levels of multiple cytokines, including IL-1β.
The expression levels of IL-6, IL-1β and TIMP-3 protein were also higher in the periodontitis group in the absence and/or presence of the P. gingivalis strains.
When comparing genotype/allele frequencies in periodontitis versus healthy and periodontitis versus gingivitis scenarios, the number of positive associations (2-4) and the degree of association (p and odds ratio values) were significantly increased by the new approach proposed (periodontitis versus gingivitis), suggesting the association of IL1B-3954, TNFA-308, IL10-592 and TLR4-299 with periodontitis risk.
One previous meta-analysis has been published on this topic and supported an association between IL-1 genes and periodontitis, but considerable doubt remains about the patient populations in which the association may be of clinical relevance.
We evaluated the expression levels of interleukins (IL-1β and IL-6), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS) in pregnant women with and without periodontal disease in comparison with non-pregnant women with and without periodontal disease since studies have suggested a relationship between periodontitis and the expression levels of these genes.