Significant Difference In IL-1β Levels Research Articles

Apical periodontitis as an aggravating factor for the severity of rheumatoid arthritis: An animal study.

The present study investigated the influence of apical periodontitis (AP) on the severity of rheumatoid arthritis (RA) using a Wistar rat model. Forty male Wistar rats were distributed across four groups (n = 10) based on the induction of RA and AP: Control, RA, AP, and RA + AP. RA was induced through two immunisations with type II collagen emulsified in incomplete Freund's adjuvant, followed by one immunisation with complete Freund's adjuvant. After 21 days of RA induction, AP was induced by exposing the pulp of four molars. Animals were euthanized after 28 days of pulp exposure. Through the experiment, visual and behavioural assessments tracked RA development and the knees and hind paw joints were measured. Micro-computed tomography scans of knees and hind paws, as well as mandibles and maxillae, were conducted to evaluate RA severity and the presence of AP, respectively. Serum samples were collected to analyse proinflammatory cytokines (IL-1β, IL-2, IL-17, and TNF-α). Non-parametric data were analysed using the Kruskal-Wallis test followed by Student-Newman-Keuls test, while one-way anova followed by Tukey's test was performed for parametric data. A significance level of 5% was employed. All molars submitted to access cavity developed AP. All joints subjected to arthritis induction developed the disease, with AP + RA demonstrating a higher arthritis severity when compared to the RA group (p < .05). RA + AP group displayed a significantly larger hind paw and knee circumference compared to the RA group (p < .05). Micro-CT images of RA and RA + AP groups revealed joints with erosions and bone deformities, with a significantly lower bone surface density, lower trabecular number and higher trabecular separation in the hind paw and a significantly lower percent bone volume and higher trabecular separation in the knees of RA + AP group compared to RA group (p < .05). RA + AP group exhibited a significantly higher level of TNF-α and a lower level of IL-2 compared to all other groups (p < .05). Both RA and RA + AP groups had significantly higher IL-17 levels (p < .05), while there was no significant difference in IL-1β levels among the groups (p > .05). The findings from this study underscore a possible relationship between apical periodontitis and the exacerbation of rheumatoid arthritis.

PENTİLENTETRAZOL İLE OLUŞTURULAN TUTUŞTURMA(KİNDLİNG) MODEL EPİLEPSİDE 5HT1 AGONİST VE ANTAGONİST'LERİNİN BEYİN TNF-ALFA VE IL1- BETA DÜZEYLERİ ÜZERİNE ETKİLERİ

Objective(s): Epilepsy is a brain dysfunction characterized by neuronal hyperexcitability and synchronized electrical discharges that cause seizures to occur. Many other neurotransmitter systems such as Serotonin (5-hydroxytryptamine, 5-HT), dopamine (DA)&nbsp;and&nbsp;adrenaline are known to be involved in the mechanism of epileptogenesis. Neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in explaining the pathophysiology of epilepsy. Inflammatory cytokine signals in the brain regulate important brain functions such as neurotransmitter metabolism, neuroendocrine function, synaptic plasticity, dopaminergic transmission, and also affect neurogenesis. This study aimed to investigate the effect of serotonin 5HT-1 agonists and antagonists on TNF-alpha (tumor necrosis factor-alpha) and IL-1 beta (interleukin-1 beta) markers in PTZ (Pentylentetrazol)-Kindling model epileptic rats. Materials and Methods: Twenty-four male Wistar albino rats of 240-280gr were used in our study. PTZ injections were done on rats on Mondays, Wednesdays, and Fridays at a dose of 35 mg/kg to create PTZ kindling model epilepsy, then, on the days of injection, the animals' behavior was observed for 30 minutes, and the stages of epilepsy were determined according to the Racine seizure stages. The animals were then divided into four groups in a randomized way: Control (n = 8) 1ml/ kg SF, 35 mg/ kg PTZ (n = 8), 0.3 mg/ kg 8-OH-DPAT (n = 8) and 1 mg/kg WAY-100135 (n = 8), which were intraperitoneal administered. After the procedure, brain tissues were dissected from the animals. Data analyses were done with SPSS for Windows version 21.0 and evaluated using one-way variance analysis (ANOVA). Results: Between the groups, IL1-β and TNF-alpha results were evaluated. The PTZ group did not change the level of IL1-β compared to the control group (p&gt;0.05), however, there was no statistically significant difference in IL1-β levels between 8-OH-DPAT and WAY-100135 groups (p&gt;0.05). Similarly, PTZ did not change the TNF-alpha level compared to the control group, and there was no statistical difference when 8-OH-DPAT, WAY-100135 groups were compared with the PTZ group (p&gt;0.05). Conclusion: In PTZ kindling epilepsy, the treatments in the 8-OH-DPA (5HT-1 agonist) and WAY-100135 (5HT-1 antagonist) groups showed no effect at TNF-alpha and IL1-β levels, despite this, more studies are needed to investigate the new therapeutic approach to treat epilepsy.

Elevated interleukin-1β in peripheral blood mononuclear cells contributes to the pathogenesis of autoimmune thyroid diseases, especially of Hashimoto thyroiditis

ABSTRACTPurpose of the study: To explore the relationship between IL-1β expression and two common autoimmune thyroid diseases: Hashimoto thyroiditis (HT) and Graves’ disease (GD). Materials and methods: qRT-PCR, Quantiglo ELISA, and flow cytometry were used to evaluate the expression levels of IL-1β in serum, peripheral blood mononuclear cells (PBMCs), and thyroid tissue samples from patients with HT or GD. Local infiltration of monocytes was assessed by immunohistochemical study of patients’ thyroid tissue samples. Results: Although no significant differences in IL-1β levels were found between samples of serum from patients with HT or GD and normal controls, we found that IL-1β mRNA and protein levels in PBMCs of HT patients were significantly higher than those of patients with GD, which were in turn higher than the level in normal controls. In addition, IL-1β mRNA was also increased in thyroid gland tissue from patients with HT compared to those with GD, and this was accompanied by increased local infiltration of monocytes into thyroid tissues. Correlation analysis of the clinical samples validated the association of high IL-1β levels with the pathogenesis of HT. Conclusion: Our study suggests that IL-1β may be an active etiologic factor in the pathogenesis of HT and thus present a new target for novel diagnostics and treatment.

Pro-inflammatory cytokines: a possible relationship with dialytic adequacy and serum albumin in peritoneal dialysis patients.

BackgroundInflammation and serum albumin concentration are both important predictors of survival in patients treated with peritoneal dialysis (PD). Furthermore, systemic and local inflammatory mediators may induce structural and functional alterations in the peritoneal membrane, thus interfering with dialysis adequacy. PD adequacy is monitored primarily by indices of small solute clearance, such as Kt/V urea and weekly creatinine clearance (wCc). The aim of this study was to investigate the possible relationship between pro-inflammatory cytokines, such as interleukin-6 (IL-6) and interleukin-1β (IL-1β), and serum albumin and C-reactive protein (CRP). Moreover, the relationship between IL-6 and IL-1β and PD adequacy has been analysed.MethodsWe enrolled 46 stable PD patients undergoing maintenance PD for a minimum of 3 months. Plasma levels of serum albumin, high-sensitivity (hs)-CRP, IL-6 and IL-1β were measured in all patients. We used weekly Kt/V urea and wCc to monitor PD adequacy. Daily urine volume was measured in all patients.ResultsThe median values of serum albumin, hs-CRP, IL-6 and IL-1β showed no significant differences between continuous ambulatory PD and automated PD patients. IL-6 levels showed a positive correlation with hs-CRP levels (P < 0.001) and a negative correlation with serum albumin concentration (P = 0.01). There was no statistically significant relationship between IL-1β and hs-CRP or serum albumin concentrations. Subsequently, PD patients were divided into two groups based on Kt/V urea value. PD patients with Kt/V ≤1.7 had significantly higher IL-6 levels compared with PD patients with Kt/V >1.7 (P = 0.015). No statistically significant relationship between IL-6 and wCc was observed. There was no significant difference in IL-1β levels between PD patients with Kt/V ≤1.7 and with Kt/V >1.7 [median (interquartile range) 0.82 (0.88–5.2) versus 1.82 (0.95–2.7)]. There was no significant difference in IL-6 and IL-1β levels in PD patients with and without residual diuresis (P = 0.32 and P = 0.77, respectively).ConclusionOur data suggest a possible relationship between serum IL-6 levels and serum albumin and hs-CRP in PD patients. Furthermore, IL-6 seems to be higher in patients with lower Kt/V, thus suggesting a possible use of this inflammatory biomarker in PD adequacy monitoring.

Interleukin-8 is involved in cervical dilatation but not in prelabour cervical ripening.

Our aim was to determine the amount and source of interleukin (IL)-8 and to study IL-8 receptor expression in the human cervix during pregnancy and after labour. Cervical biopsies were obtained from six non-pregnant women, eight women undergoing pregnancy termination, 17 women undergoing elective caesarean section and 11 women after vaginal delivery. IL-8 levels were compared in women with and without a ripe cervix, as determined by cervical Bishop score and cervicovaginal fetal fibronectin levels. Levels of IL-8 and IL-1beta, a regulator of IL-8 expression, were determined by enzyme-linked immunosorbent assay (ELISA). IL-8, IL-1beta and IL-8 receptor proteins were localized by immunohistochemistry. Compared with late pregnancy, IL-8 levels increased after labour and vaginal delivery (P < 0.01) but there was no correlation with cervical ripening. IL-8 was localized to stromal cells, macrophages and granulocytes. There were no significant differences in IL-1beta levels between groups. IL-8 receptors were expressed primarily on granulocytes and macrophages after vaginal delivery. We conclude that IL-8 is involved in cervical dilatation but not in cervical ripening.

Elevated levels of chemokines in esophageal mucosa of patients with reflux esophagitis

Objective Chemokines play a key role in the pathogenesis of various inflammatory conditions. However, there is little information on their profile in reflux esophagitis (RE). We sought to study esophageal mucosa levels of chemokines in RE. Methods A total of 32 outpatients with RE and 13 normal controls were studied. Endoscopic severity of RE was classified according to the Los Angeles grading system. Paired biopsy specimens were taken from the esophagus 3 cm above the gastroesophageal junction; one biopsy was snap frozen for measurement of mucosal levels of interleukin 8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), regulated on activation normal T-cell expressed and presumably secreted (RANTES), and IL-1β by enzyme linked immunosorbent assays, while the other was formalin-fixed for histopathological evaluation. Results IL-8, MCP-1, and RANTES levels were significantly higher in esophageal mucosa of RE patients than those of the controls. IL-8 levels correlated significantly with the endoscopic severity of RE. Basal zone hyperplasia and papillary elongation, histopathological hallmarks of RE, were both associated with higher levels of IL-8 and MCP-1. The presence of intraepithelial neutrophils and eosinophils, which also indicate RE, was associated with high levels of IL-8 and RANTES, respectively. There were no significant differences in IL-1β levels between the RE and control groups, but IL-1β levels correlated significantly with the IL-8 production. Again, the IL-8 levels were significantly decreased after lansoprazole treatment. Conclusion Our results indicate that chemokines produced locally in the esophageal mucosa may be involved in the development and progression of RE.

The Role of Tumor Necrosis Factor-α and Interleukin-1β as Predictable Markers for Development of Adult Respiratory Distress Syndrome in Septic Syndrome

Background Tumor necrosis factor(TNF)-α and Interleukin(IL)-1β are thought to play a major role in the pathogenesis of the septic syndrome, which is frequently associated with adult respiratory distress syndrome(ARDS). In spite of many reports for the role of TNF-α in the pathogenesis of ARDS, including human studies, it has been reported that TNF-α is not sensitive and specific marker for impending ARDS. But there is a possibility that the results were affected by the diversity of pathogenetic mechanisms leading to the ARDS because of various underlying disorders of the study group in the previous reports. The purpose of the present study was to evaluate the roles of TNF-α and IL-lβ as a predictable marker for development of ARDS in the patients with septic syndrome, in which the pathogenesis is believed to be mainly cytokine-mediated. Methods Thirty-six patients of the septic syndrome hospitalized in the intensive care units of the Asan Medical Center were studied. Sixteens suffered from ARDS, whereas the remaining 20 were at the risk of developing ARDS(acute hypoxemic respiratory failure, AHRF). In all patients venous blood sample were collected in heparin-coated tubes at the time of enrollment, at 24 and 72 h thereafter. TNF-α and IL-lβ was measured by an enzyme-linked immunosorbent assay (ELISA). All data are expressed as median with interquartile range. Results 1) Plama TNF-α levels: Plasma TNF-β levels were less than 10pg/mL, which is lowest detection value of the kit used in this study within the range of the mean±2SD, in all of the normal controls, 8 of 16 subjects of ARDS and in 8 in 20 subjects of AHRF. Plasma TNF-α levels from patients with ARDS were 10.26pg/mL(median;<10-16.99pg/mL, interquartile range) and not different from those of patients at AHRF(10.82, <10-20.38pg/mL). There was also no significant difference between pre-ARDS(<10, <10-15.32pg/mL) and ARDS(<10, <10-10.22pg/mL). TNF-α levels were significantly greater in the patients with shock than the patients without shock(12.53pg/mL vs. <10pg/mL) (P<0.01). There was no statistical significance between survivors(< 10, <10-12.92pg/mL) and nonsurvivors(11.80, <10-20.8pg/mL) (P=0.28) in the plasma TNF-α levels. 2) Plasma IL-lβ levels: Plasma IL-1β levels were less than 0.3ng/mL, which is the lowest detection value of the kit used in this study, in one of each patients group. There was no significant difference in IL-1β levels of the ARDS(2.22, 1.37-8.01ng/mL) and of the AHRF(2.13, 0.83-5.29ng/mL). There was also no significant difference between pre-ARDS(2.53, <0.3-8.34ng/mL) and ARDS(5.35, 0.66-11.51ng/mL), and between patients with septic shock and patients without shock (2.51, 1.28-8.34 vs 1.46, 0.15-2.13ng/mL). Plasma IL-19 levels were significantly different between survivors(1.37, 0.4-2.36ng/mL) and nonsurvivors(2.84, 1.46-8.34ng/mL). Conclusion Plasma TNF-α and IL-1β level are not a predictable marker for development of ARDS. But TNF-α is a marker for shock in septic syndrome. These result could not exclude a possibility of pathophysiologic roles of TNF-α and IL-1β in acute lung injury because these cytokine could be locally produced and exert its effects within the lungs.