Effects of smoking on the salivary and GCF levels of IL-17 and IL-35 in periodontitis.

Periodontitis progression is associated with a host response in which anti-inflammatory and pro-inflammatory cytokine networks play a key role. Smoking is involved in the production of various mediators. The study aims to evaluate the levels of IL-17 and IL-35 in saliva and gingival crevicular fluid (GCF), to investigate the effects of smoking on these cytokines in smoker and non-smoker periodontitis patients. 19 smokers with periodontitis, 20 non-smokers with periodontitis, and 18 periodontally healthy subjects were included in the study. Periodontal clinical indexes were recorded and the levels of IL-17 and IL-35 in saliva and GCF were analyzed. No significant difference was detected among the groups in terms of salivary IL-17 and IL-35 levels. GCF IL-17 and IL-35 concentration levels in the non-smoker periodontitis group were significantly lower than the others (p < 0.05). Total levels of GCF IL-17 were significantly higher in both periodontitis groups than the control group; and total levels of GCF IL-35 were significantly higher in non-smoker periodontitis group than the others (p < 0.05). A positive correlation was detected between the salivary IL-17 and IL-35 levels (r = 0.884), GCF IL-17 and IL-35 concentrations (r = 0.854), and total GCF IL-17 and IL-35 (r = 0.973) levels (p < 0.01). The present study revealed a positive correlation between the IL-35 and IL-17 levels both in saliva and GCF. IL-17 and IL-35 can be considered as one of the cytokines that play a role in periodontal health and periodontitis; and smoking may be among the factors that affect the levels of these cytokines in GCF and saliva.

Evaluation of long-term antibody kinetics in healthcare workers vaccinated with inactivated COVID-19 Vero cell vaccine (CoronaVac), a propensity score-matched observational study.

OBJECTIVES: This study aimed to evaluate the long-term antibody kinetics after vaccinating with an inactivated COVID-19 Vero cell vaccine (CoronaVac) in healthcare workers (HCWs) at a single center in Turkey. METHODS: For this prospective observational study, Chemiluminescence immunoassay (CLIA) and enzyme-linked immunosorbent assay (ELISA) were used for the determination of binding antibodies (bAb) and neutralizing antibodies (nAb), respectively. Antibody kinetics were compared for the potential influencing factors, and propensity score analysis was performed to match the subcohort for age. RESULTS: Early bAb and nAb response was achieved in all 343 participants. Titers of bAbs against SARS-CoV-2 on 42 days post-vaccination (dpv) were higher in HCWs who were aged <40 years and who had a history of COVID-19. SARS-CoV-2 bAb levels in HCWs on days 42 (n = 97), 90 (n = 97), and 180 (n = 97) were 175 IU/ml (3.9-250), 107 IU/ml (2.4-250), and 66.1 IU/ml (2.57-250), respectively (p<0.001). SARS-CoV-2 bAb (p<0.001) and nAb (p<0.001) titers decreased significantly over time. There was a high negative correlation between SARS-CoV-2 antibody titers and inverse optic density of nAb responses (Pearson correlation coefficient: -0.738, p<0.001). CONCLUSIONS: When the antibody responses were compared, it was seen that the vaccine immunogenicity was better in those who had prior COVID-19 history and were aged <40 years. In the course of time, it was determined that there was a significant decrease in bAb and nAb responses after the 90th day. These results may guide approval decisions for booster COVID-19 vaccines.

Spondylenchondrodysplasia mimicking a systemic lupus erythematosus: A diagnostic challenge in a pediatric patient.

Spondyloenchondrodysplasia (SPENCD) is a rare autosomal recessive skeletal dysplasia caused by biallelic mutations in the ACP5 gene that encodes tartrate-resistant acid phosphatase (TRAP). The extra-osseous phenotype of SPENCD is extremely pleiotropic and is characterized by neurological impairment and immune dysfunction. This phenotype can mimic systemic lupus erythematosus. Herein, we report a child presented with systemic lupus erythematosus-like symptoms, including multisystem inflammation, autoimmunity, and immunodeficiency, but was subsequently diagnosed as SPENCD.

Dendritic cell activation is blunted in patients with coronary artery disease and diabetes mellitus.

BACKGROUND: It has been shown that functional status of dendritic cells (DCs) in diabetic patients with unstable angina pectoris (UAP) are more mature and activated than diabetic patients without coronary artery disease (CAD) and none diabetic patients with UAP. Accordingly we aimed to assess the activation of DCs in patients with CAD with/and without Diabetes Mellitus (DM) and compare to those in subjects with normal coronary arteries (NCA). MATERIALS AND METHODS: Twenty three patients with severe CAD who were scheduled to coronary artery by-pass grafting surgery and 6 patients with angiographycally NCAs were included in the study. Activation of peripheral blood DCs have been analyzed by flow cytometric measures of CD86 activation. RESULTS: In patients with CAD and without DM, DC activation significantly increased after stimulation of oxidesized LDL (135 ±â€¯121 vs 248 ±â€¯197 p = 0.024). However this activation didn't significantly increased in patients with CAD and DM (100 ±â€¯20 vs 120 ±â€¯97, p = 0,54). Patients with NCAs and without DM showed marked activation of CD86 after stimulation with ox-LDL. CONCLUSION: We have documented that DC activation, upon stimulation of ox-LDL has blunted in patients with CAD compared to patients with NCAs. Moreover this defective activation is more pronounced in those with diabetic patients with CAD.

Correlation between IL-17A/F, IL-23, IL-35 and IL-12/-23 (p40) levels in peripheral blood lymphocyte cultures and disease activity in Behcet's patients.

Behcet's disease is a chronic multisystemic disease with remissions and relapses. Several studies have shown that immune mechanisms play an important role in the development of the disease. In order to assess the association of disease activity with IL-17A/F, IL-23, IL-12/23 (p40) and IL-35 expression, we aimed to investigate production of these cytokines in peripheral blood mononuclear cells (PBMCs) from Behcet's patients and normal controls. Furthermore, we included Systemic Lupus Erythematosus (SLE) as disease control to evaluate the specificity of our data for immunopathogenesis of BD. Totally 15 active, 15 inactive Behcet's patients, 12 active and 12 inactive SLE patients and 12 healthy volunteers were enrolled in the study. Peripheral blood mononuclear cells were separated, lymphocyte cultures were performed and IL-17A/F, IL-12/23 p(40), IL-23, IL-35 cytokine levels were measured by ELISA in culture supernatants in the presence or absence of phytohemagglutinin (PHA) on time-dependent manner. IL-17 A/F levels increased parallel to IL-23 levels in Behcet's and SLE patients. Compared to healthy controls, IL-17 A/F levels were higher in active Behcet's and SLE patients; on the contrary, levels of IL-35 were lower. IL-17A/F, IL-12/23 (p40) and IL-23 levels were detectable most frequently in active Behcet's patients followed by active SLE patients. Our results indicate that IL-17 A/F, IL-23 and IL-12/23 (p40) may play role in the immunopathogenesis of BD so as Th17 and Th1 cell responses. Since IL-35 levels were lower in active Behcet's patients compared to inactive patients and healthy controls, there may be a plasticity between Th17 and Treg cells according to the state of disease activity.

The importance of serum biglycan levels as a fibrosis marker in patients with chronic hepatitis B.

BACKGROUND: Liver biopsy is recommended in the majority of patients with chronic viral hepatitis for fibrosis evaluation. Because of the potential risks of liver biopsy, many studies related to non-invasive biomarkers of hepatic fibrosis have been performed. We aimed to assess the diagnostic value of serum biglycan as a non-invasive fibrosis marker in chronic hepatitis B patients. METHODS: This study included 120 patients with biopsy-proven hepatitis B patients and 60 healthy controls. Fibrosis stage and necroinflammatory activity were assessed in liver biopsy specimens. Biglycan level was measured using an ELISA assay. RESULTS: Serum biglycan levels of chronic hepatitis B patients were found to be significantly higher than those of healthy controls (337.3±363.0 pg/mL vs 189.1±61.9 pg/mL, respectively, P<.001). There was a statistically significant positive correlation between serum biglycan level and fibrosis stage (P=.004; r=.213). Besides, a statistically significant positive correlation was found between serum biglycan level and necroinflammatory activity (P<.001; r=.271). The AUROC of BGN levels was 0.702 for fibrosis stage, differentiating patients from healthy controls with statistical significance (P<.001). The AUROC of BGN levels was 0.632 for necroinflammatory activity score, differentiating patients from healthy controls with statistical significance (P=.004). CONCLUSIONS: Serum biglycan might be used as a non-invasive marker of liver fibrosis. Further studies are needed to evaluate the usefulness of this marker.

Primary Sjögren's syndrome is associated with significant cognitive dysfunction.

AIM: Cognitive dysfunction is a neurologic manifestation in primary Sjögren syndrome (PSS). On the other hand, several antibodies are related to cognitive dysfunction. The aim of this study is to assess the cognitive dysfunction of PSS patients via detailed neurologic tests. Moreover, its associations with antibodies were also evaluated. METHOD: Twenty-eight female patients with PSS and 17 healthy controls comprised the study groups. Short-term memory, long-term memory, verbal learning, visual memory, visual spatial perception, attention, verbal frequency function, executive functions and information processing speed were evaluated with neurologic tests in both of the study groups. Furthermore, anti-N-methyl-D-aspartate (NMDA) type anti-glutamate-receptor antibody, anti-ribosomal-p and antiganglioside antibodies were assessed in the study groups. RESULTS: The attention, data processing speed, verbal learning, short-term verbal memory and visuo-spatial perception performances were lower in the patients with PSS when compared to the healthy controls. The difference reached statistical significance in Paced Auditory Serial Addition Test (P < 0.01), Serial Digit Learning Test (P < 0.01), clock drawing (P = 0.03), Auditory Verbal Learning Test immediate verbal memory (P = 0.01) and Benton Judgement of Line Orientation Test (P = 0.03). Even if antiganglioside antibodies were more likely to be present in the PSS group when compared to the healthy controls, no relationship was found between its positivity and cognitive dysfunction. CONCLUSION: Results of this study suggest that cognitive dysfunction is quite prevalent in PSS patients without being associated with studied antibodies.

Serum Cytokine Profiles in Infants with Atopic Dermatitis.

Atopic dermatitis (AD) in infancy is believed to have distinct features as compared to AD in other age groups, and little is known about cytokine production in infants with AD. We aimed to measure the serum cytokine levels of infants with atopic dermatitis and evaluate the association of new anti-inflammatory cytokines with the disease. Eighty-one infant patients with AD and 52 healthy controls were involved in this study. The serum levels of major pro- and anti-inflammatory cytokines of the T-helper (Th) subtypes, as well as more recently defined interleukins (IL-27, IL-35, and IL-37), were measured using the ELISA method. The serum levels of IL-35, IL-5, and interferon (IFN)-γ were found to be significantly higher, while the levels of transforming growth factor (TGF)-ß1 and IL-13 were found to be significantly lower in patients with AD as compared to controls. There was no statistically significant correlation between serum cytokine levels and objective SCORAD index or total immunoglobulin (Ig) E levels. We did not observe prominent serum Th2 polarization in atopic infants. The immunopathogenesis of atopy onset at an early age may be more complicated than that at older ages.

Can serum pin1 level be regarded as an indicative marker of nonalcoholic steatohepatitis and fibrotic stages?

BACKGROUND: We aimed to investigate serum Pin1 as an indicator of the presence of nonalcoholic steatohepatitis (NASH) and its association with the histopathological liver fibrosis stages. METHODS: Serum samples were collected from consecutive biopsy-proven NASH patients and healthy controls, and then serum levels of Pin1 were measured. The correlations between clinical and histopathological features of NASH and Pin1 were evaluated. Patients who had fibrotic stages <2 were termed mild fibrosis group and those who had ≥ 2 as advanced fibrosis group. We performed univariate and multivariate logistic regression analyses to evaluate the independent predicting factors for the presence of liver fibrosis caused by NASH. RESULTS: Fifty-six consecutive NASH patients and 56 age- and sex-matched healthy controls were enrolled in the study. Serum Pin1 levels were significantly higher in NASH patients (39.24 ± 30.94) than in controls (27.7 ± 9.56, p < 0.001). In NASH patients, serum Pin1 levels were correlated with the histopathological features. Patients with advanced fibrosis had higher serum Pin1 levels than the mild fibrosis group (53.42 ± 33.8 vs. 33.24 ± 20.90, respectively; p < 0.001). In multivariate analysis, Pin1 remained an independent predicting factor of advanced liver fibrosis (OR: 1.051, 95% CI: 1.013-1.089, p < 0.05). CONCLUSION: Serum Pin1 level can be used as a potential independent marker of the presence of the NASH and advanced fibrotic scores.

Short term effects of non-surgical periodontal treatment on gingival crevicular fluid levels of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 2 (PAI-2) in patients with chronic and aggressive periodontitis.

OBJECTIVE: The purpose of this study was to evaluate the gingival crevicular fluid (GCF) levels of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor 2 (PAI-2) in aggressive periodontitis (AgP), chronic periodontitis (CP) and periodontally healthy control subjects, before (BT) and after (AT) the non-surgical periodontal treatment. DESIGN: Systemically healthy 12 CP and 13 AgP patients and 20 control subjects were included in this study. Plaque index, gingival index, probing depth and clinical attachment levels were recorded and GCF samples were collected BT and AT. Assays for GCF t-PA and PAI-2 levels were carried out by an enzyme linked immunosorbent assay (ELISA). The χ(2), Wilcoxon and Mann-Whitney U tests and Spearman correlation coefficient were used for data analyses. RESULTS: Statistically significant reductions in clinical index scores were noted in both periodontitis groups after treatment. No significant differences were detected in GCF levels of t-PA and PAI-2 between CP and AgP groups at either BT or AT. There was a statistically significant decrease in GCF PAI-2 levels in CP after therapy (p<0.01). GCF t-PA levels in CP and AgP groups exhibited significant correlations with PD and CAL measurements at both BT and AT (p<0.01). CONCLUSION: Significant decrease was detected for GCF PAI-2 levels in CP and clinical parameters in both CP and AgP by non-surgical periodontal treatment.