Effect of interleukin-12 gene expression on insulin resistance in patients with acne vulgaris.

BACKGROUND: Insulin resistance (IR) is a condition where cells become resistant to insulin, causing impaired glucose uptake and increased blood glucose levels. Interleukin-12 (IL-12), a cytokine, regulates the immune system. High levels of IL-12 can lead to chronic inflammation, exacerbate resistance to insulin, and contribute to type 2 diabetes. Also, link IR to acne vulgaris (AV), as it reduces tissue sensitivity to insulin, causing increased insulin levels and sebum production, which can contribute to acne development. AIM: To explore the role of IL-12 gene expression on IR in AV patients and to study the role of IL-12 gene in the development of AV. SUBJECTS AND METHODS: A case-control study was performed on 68 AV patients and 68 healthy controls. The biochemical analysis included fasting glucose, fasting insulin, (HOMA-IR), and serum IL-12 level. IL-12 gene expression was performed by quantitative real-time PCR for both two groups. In addition, folding change was calculated by using the standard 2-(∆∆Ct) method. RESULT: IL-12 level, IL-12 folding change, fasting insulin, and IR were all increased in acne patients. A highly significant linear correlation was found between IL-12 folding change and both IL-12 levels and IR. There is a substantial positive significant simple linear association between IL-12 level and IL-12 folding change, as well as IR and IL-12 folding change, in moderate and severe acne. CONCLUSION: IL-12 gene has an important role in IR and the development of acne in AV patients.

Genetic variants in IL12 influence both hepatitis B virus clearance and HBV-related hepatocellular carcinoma development in a Chinese male population.

IL12 plays a major role not only in inducing appropriate immune responses against viral infections (including HBV) but also in the antitumor immune response. This study was conducted to investigate the relationships of genetic variants in IL12 with hepatitis B virus (HBV) clearance and development of HBV-related hepatocellular carcinoma (HCC). We genotyped three single nucleotide polymorphisms (SNPs) of the IL12A (rs568406 and rs2243115) and IL12B (rs3212227) in 395 HBV-positive HCC patients, 293 persistent HBV carriers and 686 subjects with HBV natural clearance from southern China, using the improved multiplex ligase detection reaction (iMLDR) method. Logistic regression analysis adjusted for age, smoking, and alcohol consumption status showed that rs568408 variant genotypes were significantly associated with host HBV-related HCC risk when compared with persistent HBV carriers, and carriers of the GA + AA genotype decreased the HCC risk in comparison with GG carriers (adjusted OR = 0.53, 95 % CI 0.35-0.80, P = 0.002). No relationships between the rs2243115 and rs3212227 SNPs and HCC risk were observed (all P > 0.05). Besides, rs568408 showed an approaching significant effect on susceptibility to HBV persistent infection (adjusted OR = 1.34, 95 % CI 0.99-1.81, P = 0.057 in dominant genetic models). Furthermore, the TG haplotype was observed to be associated with a significantly increased risk of HBV-related HCC (OR = 1.42, 95 % CI 1.10-1.83, P = 0.006), while TA haplotype was associated with a decreased risk of HBV-related HCC (OR = 0.61, 95 % CI 0.45-0.83, P = 0.002). Our results reveal that the IL12A rs568408 variant may be a marker SNP for risk of both HBV clearance and HBV-related HCC development.

The Effects of Smoking on Expression of IL-12 and IL-1ß in Gingival Tissues of Patients with Chronic Periodontitis.

AIM: The purpose of this study was to compare IL-1ß and IL-12 gene expression in the gingival tissue of smokers and non-smokers either with healthy periodontium or with chronic periodontitis. MATERIALS AND METHODS: 41 individuals consisting of 21 healthy controls (11 non-smokers and 10 smokers) and 20 chronic periodontitis patients (10 non-smokers and 10 smokers) participated in this study. Samples were collected from papillary regions of targeted areas and cytokines were analyzed using Real Time PCR. Shapiro-Wilk, Mann-Witney and Independent T tests were employed for statistical analysis. RESULTS: IL-1ß gene expression in gingival tissue of non-smoker group with chronic periodontitis was significantly higher than non-smoker-healthy group (p=0.011). Smoker-chronic periodontitis group showed lower IL-1ß gene expression than non-smoker-chronic periodontitis group (p=0.003). IL-12 gene expression was not significantly different between analyzed groups. CONCLUSION: IL-1ß gene expression increases in gingival tissue of non-smoker-chronic periodontitis patients due to inflammatory processes but smoking reduces the expression of this cytokine in diseased periodontal tissues. On the other hand periodontal condition and smoking habits do not seem to affect IL-12 gene expressions in gingival tissues. Authors concluded that reduced levels of IL1 and in some extent IL12 in smoking patients are responsible for higher tissue and bone degenerations and less treatment responses in smokers.