Journal of Interferon and Cytokine Research最新文献

Toll-like receptors (TLRs), particularly the TLR2, take part in the elicitation of immune responses against Entamoeba histolytica. This study aimed to investigate the relationship between a specific polymorphism called rs3804099 in the TLR2 gene and E. histolytica/E. dispar/E. moshkovskii infection among Lebanese children. A case-control study encompassed 180 participants including 68 children with amebiasis and 112 matched controls. Blood samples were collected, and genomic DNA was extracted using the classical proteinase K digestion and phenol-chloroform extraction method. The variant rs3804099 was examined using the Amplification Refractory Mutation System Polymerase Chain Reaction. The accuracy of the genotyping was supported by sequencing 5% of samples. The TLR2 rs3804099 polymorphism was identified in the studied population, and the observed genotypic distributions were consistent with Hardy-Weinberg equilibrium (P > 0.05). The frequency of the rare CC genotype was significantly higher in patients compared to the noninfected group (P < 0.01). In controls, the homozygous TT genotype was less frequent than the heterozygous CT genotype. The rare CC genotype was associated with a higher risk of amebiasis among children (odds ratios = 3.27, P = 0.002). These findings provide evidence supporting the association between the rs3804099 SNP in the TLR2 gene and E. histolytica/E. dispar/E. moshkovskii infection among Lebanese children.

This study aimed to validate an inflammation-based risk score in patients with ST-segment elevation myocardial infarction (STEMI) by examining their cytokine profiles. Upon admission, patients were evaluated for systemic inflammation using a risk score that assigned points based on specific biomarkers: 1 point for leukocyte count ≥9.3 × 10³ cells/μL, 2 points for high-sensitivity C-reactive protein (hsCRP) ≥13.0 mg/L, and 3 points for serum albumin ≤3.6 g/dL. Patients were categorized into three groups: no inflammation (0 points, n = 13), mild inflammation (1-2 points, n = 35), and severe inflammation (3-6 points, n = 26). Serum levels of 16 key cytokines were measured. Patients with higher risk scores showed elevated interleukin (IL)-6 levels (19.6 vs. 8.5 vs. 6.8 pg/mL; P = 0.021) and decreased interferon-γ-induced protein-10 (IP-10) levels (73.4 vs. 68.8 vs. 112.2 pg/mL; P = 0.011). IL-6 was positively correlated with hsCRP (ρ 0.307) and negatively correlated with albumin (ρ -0.298), while IP-10 was negatively correlated with leukocyte count (ρ -0.301). No other cytokines showed significant association with the risk score. Higher inflammation scores were also associated with an increased incidence of major adverse cardiovascular events, particularly acute heart failure. This study underscores the association between the inflammation-based risk score and cytokine levels, specifically IL-6 and IP-10, in patients with STEMI.

Metabolic alterations are a common problem in people living with HIV (PLHIV), as a result of a stage of chronic inflammation that affects the homeostasis of the organism. Prolonged exposure to antiretroviral therapy has been associated with developing lipodystrophies that modify lipoprotein metabolism and inflammatory markers such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which are mediators of the immune response. The study aimed to associate TNF-α and IL-6 levels with their polymorphisms and metabolic alterations in PLIHV. We hypothesized that TNF-α and IL-6 levels and their polymorphisms are associated with metabolic alterations. In total, 185 PLHIV and 51 HIV-negative people were included. Biochemical parameters were determined by colorimetric assay, cytokine levels by immunoassay, and allelic discrimination by quantitative polymerase chain reaction. A correlation was found between TNF-α levels and the variables cholesterol (r = -0.171, P = 0.020) and high-density lipoprotein (HDL) (r = -0.245, P = 0.001). There are associations between HDL levels (P = 0.011) and GG genotype of rs1800629. The results suggest a metabolic alteration related to the constant immune response, especially the production of proinflammatory cytokines such as TNF-α and IL-6. It was observed that genetic factors may influence metabolism alteration, mainly in lipids.

Interferon lambdas (IFN-λs) are crucial to control virus infections at mucosal surfaces. Interleukin-22 (IL-22) was reported to help IFN-λ control rotavirus infection in the intestinal epithelium of mice either by aiding in the induction of interferon-stimulated genes (ISGs) or by increasing cell proliferation thereby clearing virally infected cells. We investigated whether IL-22 and IFN-λs exhibit similar synergistic effects in human intestinal epithelial cells (IECs) models. Our results showed that co-treatment of IL-22 and IFN-λ induced more phosphorylation of STAT1 than either cytokine used alone. However, this increased STAT1 activation did not translate to increased ISGs production or antiviral protection. Transcriptomics analysis revealed that despite sharing a common subunit (IL-10Rb) within their heterodimeric receptors and activating similar STATs, the signaling generated by IL-22 and IFN-λs is independent, with IFN-λ signaling inducing ISGs and IL-22 signaling inducing cell proliferation genes. Using human intestinal organoids, we confirmed that IL-22 increased the size of the organoids through increased cell proliferation and expression of the stem cell marker (OLFM4). These findings suggest that in human intestinal cells, IFN-λs and IL-22 act independently to clear virus infections. IFN-λs induce ISGs to control virus replication and spread, whereas IL-22 increases cell proliferation to eliminate infected cells and repair the damage epithelium. Although these two cytokines do not act synergistically, each plays a key function in the protection of human IECs.

Bronchial asthma (BA) is increasing among Egyptian children. It is affected by multiple factors including genetic ones. In the current study, we assessed the relationship between interleukin-17 (IL-17) genotypes and the occurrence of BA among Egyptian children. This case-control study included 100 participants. Group I (the control group) comprised 50 healthy subjects. Group II (the asthmatic group) comprised 50 subjects diagnosed with atopic asthma according to the Global Initiative for Asthma. Measurement of serum Ig E and eosinophilic count was performed. Detection of single nucleotide polymorphism rs2275913 of IL-17 gene by restriction fragment length polymorphism-polymerase chain reaction was conducted. GA and AA genotypes were more frequent in the asthmatic group compared to the control group (P = 0.03 and 0.01, respectively). Subjects carrying GA and AA genotypes were more susceptible to have asthma [odds ratio (OR) = 2.21, 95% confidence interval (CI) = 1.14-9.94, P = 0.03; OR = 7.78, 95% CI = 1.59-38.3, P = 0.01, respectively]. The A allele was higher in the asthmatic group (33%) compared to the control group (10%). A allele carriers were more susceptible to have asthma (OR = 4.43, 95% CI = 2.04-9.82 and P < 0.001). Immunoglobulin E (IgE) levels and eosinophil percentages were higher among the carriers of GA and AA genotypes when compared with the GG genotype. All pulmonary function tests were significantly lower among carriers of AA genotype compared with GG genotype. An A allele carrier, AA genotype, increased IgE level, and eosinophil level were significant predictors for occurrence of asthma (P = 0.01, 0.02, 0.004, and 0.01). In conclusion, AA genotype carriers and A allele carriers of the IL-17 gene are more likely to have asthma compared with controls.

Adenohypophysis-inducible sex hormones include prolactin (PRL), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). These hormones influence the occurrence of lupus erythematosus by affecting the endocrine and immune systems. The present study analyzed the relationship between serum sex hormones and several cytokines in patients with systemic lupus erythematosus (SLE). Compared with the healthy controls, early-onset SLE female patients with menopause had higher PRL levels than the healthy controls and cutaneous lupus erythematosus (CLE) group. FSH levels were higher in male patients with SLE than in the healthy controls or CLE group. In SLE patients, the estradiol levels correlated negatively with interleukin (IL)-8. The levels of FSH versus IL-8, PRL versus IL-6, PRL versus tumor necrosis factor (TNF)-α, and LH versus IL-8 levels were moderately positively correlated. In conclusion, PRL, FSH, and LH are positively associated with IL-6, IL-8, and TNF-α in the sera from SLE patients, which indicates that sex hormone levels can serve as an indicator of disease activity during SLE diagnosis.

Interleukin-26 (IL-26) is a cytokine that belongs to the IL-20 subfamily and is primarily expressed in T helper 1 cells and Th17 memory CD4⁺ cells. Its receptor complex, consisting of IL-20R1 and IL-10R2, activates a signaling pathway involving several proteins such as Janus kinase 1 and tyrosine-protein kinase, signal transducer and activator of transcription (STAT) 1, and STAT3. This leads to the initiation of downstream signaling cascades that play a crucial role in various biological processes, including inflammation, immune response regulation, atopic dermatitis, macrophage differentiation, osteoclastogenesis, antibacterial host defense, anti-apoptosis, and tumor growth. In this study, we curated literature data pertaining to IL-26 signaling. The curated map includes a total of seven activation/inhibition events, 16 catalysis events, 33 gene regulation events, 25 protein expression types, two transport events, and three molecular associations.