Immunoinflammatory Markers Research Articles

Association of blood count–derived immunoinflammatory makers and risk of epilepsy: A prospective cohort of 497,291 participants

ObjectiveTo explore the longitudinal association between blood count-derived immunoinflammatory markers and the risk of epilepsy in a large population cohort. MethodsWe used data from the UK Biobank (UKB) to investigate the association between pre-diagnostic peripheral immunoinflammatory cells and their derived ratios, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), and the risk of epilepsy. This was a longitudinal cohort study in which multivariate Cox proportional hazards models and a series of sensitivity and subgroup analyses were performed to explore the nature of these associations. ResultsWe examined these associations in a prospective UKB cohort of 497,291 participants. During a median follow-up of 12.43 years, 2,715 participants developed epilepsy. After adjusting for all covariates, the results showed that higher monocyte counts and some blood count-derived immunoinflammatory metrics (monocyte counts, hazard ratio [HR]=1.093, 95 % confidence interval [CI] 1.052–1.136, P<0.001; NLR, HR=1.062, 95 % CI 1.022–1.103, P=0.002; PLR, HR=1.096, 95 % CI 1.055–1.139, P<0.001; SII, HR=1.041, 95 % CI 1.003–1.082, P=0.036) were associated with an increased risk of epilepsy. Conversely, we found that higher lymphocyte counts and LMR were negatively associated with the risk of epilepsy (lymphocyte count, HR=0.889, 95 % CI 0.856–0.923, P < 0.001; LMR, HR=0.85, 95 % CI 0.82–0.881, P < 0.001). ConclusionsMonocyte count, NLR, PLR, and SII increased the risk of epilepsy, whereas lymphocyte count and LMR decreased it. Further studies will help translate these findings into clinical practice or targeted treatments.

The First Comprehensive Evaluation of Immuno-Inflammatory Markers for Prognosis in Esophageal Cancer Patients: A South Asian Perspective.

Background: Esophageal cancer (EC) remains a significant health challenge in South Asia, with poor prognosis despite advancements in diagnostics and treatment. Identifying and validating prognostic factors is essential for improving patient outcomes. Methods: A prospective study was conducted with 146 biopsy-confirmed EC patients at the Dr. Ruth K.M. Pfau Civil Hospital, Karachi, Pakistan. Clinical and laboratory data were collected and analyzed using descriptive statistics, receiver operating characteristic (ROC) analysis, and the Chi-square test. Survival outcomes were assessed using Kaplan-Meier curves, log-rank tests, and Cox proportional hazard models for univariate and multivariate regression analyses, with statistical significance set at p ≤ 0.05. Results: Bivariate analysis showed significant associations of the neutrophil lymphocyte ratio (NLR) (p = 0.017), C-reactive protein to albumin ratio (CAR) (p = 0.033), red cell distribution width to platelet ratio (RPR) (p = 0.020), and systemic immune-Inflammation index (SII) (p = 0.009) with patient survival. Univariate analysis identified tumor length >10 cm (p = 0.016), T4 stage (p = 0.015), metastasis (p < 0.001), surgery not performed (p < 0.001), and SII (p = 0.022) as significant factors for survival, with higher SII linked to poorer overall survival (p = 0.020). Interestingly, in the multivariate model, only metastasis (p < 0.001) and surgery not performed (p = 0.011) remained significant. Conclusions: Immuno-inflammatory markers may be less pertinent prognostic factors for EC in the South Asian population.

N6‑methyladenosine methyltransferase METTL14 is associated with macrophage polarization in rheumatoid arthritis.

Rheumatoid arthritis (RA) is largely caused by the inflammatory response triggered by macrophage polarization. Through epigenetic reprogramming, the inflammatory state of macrophages can be modified. Macrophage polarization is associated with the RNA epigenetic alteration N6-methyladenosine (m6A) RNA methylation. However, the specific function and underlying mechanisms of m6A methylation in the role of macrophage polarization in RA remain to be elucidated. The mRNA expression levels of m6A methylase genes and signaling pathway components associated with RA macrophages were determined in the present study using reverse-transcription quantitative PCR. Methyltransferase 14 (METTL14) protein expression levels were determined using western blot analysis, and the levels of specific cellular secretion factors were determined using ELISA and flow cytometry. The results of the present study demonstrated that elevated METTL14 expression was associated with joint tenderness, and METTL14 expression was positively correlated with both C-reactive protein and rheumatoid factor expression levels. Moreover, METTL14 exhibited potential in the prediction of visual analogue scale. Pro-inflammatory cytokines (TNF-α) and M1 macrophage markers (CD68+CD86+) were also positively associated with METTL14 expression. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that METTL14 was strongly associated with the MAPK signaling pathway. Notably, JNK and ERK2 exhibited a positive correlation with the M1 macrophage marker, CD68+CD86+, which was positively associated with the pro-inflammatory factor, TNF-α. JNK and ERK2 expression levels were markedly increased in the METTL14 high-expression group, compared with in the low-expression group; however, p38 and ERK1 expression levels were not significantly different between these groups. Collectively, the results of the present study demonstrated that METTL14 expression was significantly increased in the peripheral blood and synovial tissue of patients with RA, highlighting the potential association with both immunoinflammatory markers and clinical symptoms. In addition, it was suggested that METTL14 may exacerbate the downstream inflammatory response, through mediating macrophage polarization via the MAPK pathway.

Abstract P343: Cerebral injury and cognitive performances are correlated with immunoinflammatory markers in hypertensive patients

Immunity and inflammation play a pivotal role in hypertension onset and cardiovascular organ damage. This role has been thoroughly characterized for classical hypertension targets as the kidneys, the heart and the vasculature. Many studies have characterized this in the experimental context, however immunoinflammatory challenges links with brain injury in the clinical context of hypertension are still lacking. In this study we will characterize how immunoinflammatory mediators can be predictors of cerebral injury characterized by advanced neuroimaging in hypertensive patients. Hypertensive patients underwent cerebral MRI and by advanced neuroimaging we characterized the microstructural injury by DTI fiber tracking. We administered the Montreal Cognitive Assessment to evaluate cognitive function, measured circulating C-reactive protein (hs-CRP) and counted circulating white blood cells (WBC). We found a large cluster of white matter tracts whose integrity parameters were associated with immunoinflammatory biomarkers (Figure A). In particular, a cluster of tracts of the limbic system and encompassing the corpus callosum show a correlation between their loss of integrity and hs-CRP levels. Another cluster of associative tracts spanning the temporal lobe show association between their loss of integrity and the WBC. Finally, the Frontal Aslant and the Uncinate Fasciculus show association with both immunoinflammatory markers (Figure B). In this study we performed advanced neuroimaging analyses to characterize the interplay between immunoinflammatory risk and cerebral alterations in hypertensives. Furthermore, our previous work identified that white matter damage in the Forceps Minor and Superior Longitudinal Fasciculus was a typical trait of hypertensive patients and associated to loss of cognitive functions. Our data further show the inflammatory risk association with worse cognitive functions, suggesting a clinical relevance in terms of damage evidenced by advanced MRI in hypertensive patients.

Pan-immune-inflammation value: a new prognostic index in epithelial ovarian cancer

BackgroundEpithelial ovarian cancer (EOC) is one of the deadliest gynaecological malignancies worldwide. The aim of this retrospective study was to create a predictive scoring model based on simple immunological and inflammatory parameters to predict overall survival (OS) and progression-free survival (PFS) in patients with EOC.MethodsWe obtained 576 EOC patients and randomly assigned them to the training set (n = 405) and the validation set (n = 171) in a ratio of 7:3. We retrospectively evaluated the association between PIV and OS and PFS using a novel immunoinflammatory marker, according to the optihmal treshold of PIV, we divided the patients into two different subgroups, high PIV (PIV > 254.9) and low PIV (PIV ≤ 254.9). Pan-immune Inflammatory Value (PIV) was computed as follows: neutrophil count (109/L) × platelet count (109/L) × monocyte count (109/L)/lymphocyte count (109/L). Then developed a simple score prediction model based on several independent prognostic parameters using Cox regression analysis. We used receiver operator characteristic (ROC) curves, calibration plots, and decision analysis (DCA) curves to evaluate the performance of the model. Finally, we used Kaplan-Meier curves to ensure that the model could distinguish well between low- and high-risk groups.ResultsThere was a significant difference in survival outcomes between high PIV (PIV > 310.2) and low PIV (PIV ≤ PIV310.2) (3-year survival rates of 61.34% and 76.71%, respectively); 5-year OS, 25.21% and 51.14%, respectively; 3-year PFS, 40.90% and 65.30%; 5-year PFS, 19.33% and 39.73%, respectively). Column plots of OS and PFS were constructed using independent prognostic factors. In the training module, the 3-, 5-, and 10-year AUCs for OS and PFS column charts were 0.713, 0.796, 0.839, and 0.730, 0.799, 0.826, respectively.In the validation cohort, the 3-, 5-, and 10-year AUCs for OS and PFS column charts were 0.676, 0.803, 0.685, and 0.700, respectively, 0.754, 0.727. The calibration curves showed good agreement between predicted survival and actual observations. The decision analysis curves also showed that the current model has good accuracy and clinical applicability. 3-year OS was 61.34% and 76.71%, respectively; 5-year OS was 25.21% and 51.14%, respectively; 3-year PFS was 40.90% and 65.30%, respectively; 5-year PFS was 19.33% and 39.73%, respectively.ConclusionsWe constructed and validated a PIV-based nomogram to predict OS and PFS in EOC patients, with a view to helping gynaecologists converge on oncologists in their treatment and follow-up expertise in epithelial ovarian cancer.

Predictive ability of complete blood count, mean platelet ratio, mean platelet volume, and neutrophil/lymphocyte ratio for severe pneumonia among RT-PCR or radiologically proven COVID-19 patients.

Immuno-inflammatory markers related to white blood cells, and platelets are shown to be associated with COVID-19 infection, and considered to be independent markers for clinical outcomes and mortality. The present study aimed to study the predictive value of these hematologic parameters in progression of COVID-19 to severe pneumonia. This was an analytical cross-sectional study conducted among RT-PCR or radiologically proven COVID-19 patients in a tertiary care hospital in Rajasthan. Semi-structured questionnaire was used to collect the epidemiological information of the patients with COVID-19. Complete blood count and other laboratory parameters were also studied among the patients. Mean age of participants in the study was 52 years, with about 70% being males. Cough and breathlessness were the most common symptoms among the patients. It was found that the parameters related to white blood cells were significantly different between patients with COVID-19 infection and severe pneumonia (except absolute monocyte count). NLR was significantly higher among those with severe pneumonia. In the univariate analysis, age (OR - 1.02), NLR (OR - 1.16), and albumin (OR - 0.45) were found to be significant predictors of progression to severe pneumonia. In the final model, adjusted for confounders, only NLR and albumin levels significantly predicted progression to severe pneumonia among COVID-19 patients. The study consolidates the predictive ability of NLR for severe pneumonia. It is an important finding, as health facilities with limited access to laboratory investigations can rely on simple markers in routine practice to predict the progression of COVID-19 infection to severe pneumonia.

Titanium dioxide nanotubes applied to conventional glass ionomer cement influence the expression of immunoinflammatory markers: An in vitro study

ObjectivesTo assess the impact of different concentrations TiO2-nt incorporated into a glass ionomer cement on the proliferation, mitochondrial metabolism, morphology, and pro- and anti-inflammatory cytokine production of cultured fibroblasts (NIH/3T3), whether or not stimulated by lipopolysaccharides (LPS-2 μg/mL, 24 h). MethodsTiO2-nt was added to KM (Ketac Molar EasyMix™, 3 %, 5 %, 7 % in weight); unblended KM was used as the control. The analyses included: Cell proliferation assay (n = 6; 24/48/72h); Mitochondrial metabolism assay (n = 6; 24/48/72h); Confocal laser microscopy (n = 3; 24/48/72h); Determination of biomarkers (IL-1β/IL-6/IL-10/VEGF/TNF) by using both multiplex technology (n = 6; 12/18 h) and the quantitative real-time PCR assay (q-PCR) (n = 3, 24/72/120 h). The data underwent analysis using both the Shapiro-Wilk and Levene tests, and by generalized linear models (α = 0.05). ResultsIt demonstrated that cell proliferation increased over time, regardless of the presence of TiO2-nt or LPS, and displayed a significant increase at 72 h; mitochondrial metabolism increased (p < 0.05), irrespective of exposure to LPS (p = 0.937); no cell morphology changes were observed; TiO2-nt reverted the impact of KM on the secreted levels of the evaluated proteins and the gene expressions in the presence of LPS (p < 0.0001). ConclusionsTiO2-nt did not adversely affect the biological behavior of fibroblastic cells cultured on GIC discs.

Association between multiple-heavy-metal exposures and systemic immune inflammation in a middle-aged and elderly Chinese general population

BackgroundExposure to heavy metals alone or in combination can promote systemic inflammation. The aim of this study was to investigate potential associations between multiple plasma heavy metals and markers of systemic immune inflammation.MethodsUsing a cross-sectional study, routine blood tests were performed on 3355 participants in Guangxi, China. Eight heavy metal elements in plasma were determined by inductively coupled plasma mass spectrometry. Immunoinflammatory markers were calculated based on peripheral blood WBC and its subtype counts. A generalised linear regression model was used to analyse the association of each metal with the immunoinflammatory markers, and the association of the metal mixtures with the immunoinflammatory markers was further assessed using weighted quantile sum (WQS) regression.ResultsIn the single-metal model, plasma metal Fe (log10) was significantly negatively correlated with the levels of immune-inflammatory markers SII, NLR and PLR, and plasma metal Cu (log10) was significantly positively correlated with the levels of immune-inflammatory markers SII and PLR. In addition, plasma metal Mn (log10 conversion) was positively correlated with the levels of immune inflammatory markers NLR and PLR. The above associations remained after multiple corrections. In the mixed-metal model, after WQS regression analysis, plasma metal Cu was found to have the greatest weight in the positive effects of metal mixtures on SII and PLR, while plasma metals Mn and Fe had the greatest weight in the positive effects of metal mixtures on NLR and LMR, respectively. In addition, blood Fe had the greatest weight in the negative effects of the metal mixtures for SII, PLR and NLR.ConclusionPlasma metals Cu and Mn were positively correlated with immunoinflammatory markers SII, NLR and PLR. While plasma metal Fe was negatively correlated with immunoinflammatory markers SII, NLR, and PLR.

Effect of Unmetabolized Folic Acid on Immunoinflammatory Markers in Sickle Cell Disease Patients Taking Folic Acid Supplementation.

Folic acid (FA) supplementation in sickle cell disease (SCD) patients lead to accumulation of unmetabolized folic acid (UMFA) which might influence the level of cytokines and NK cell activity and thus trigger the crisis event. The aim of the study was to investigate the effect of UMFA levels on immuno-inflammatory markers in SCD patients taking FA supplementation. The cross-sectional study was conducted on 60 HbSS confirmed SCD cases with 22 crisis and 38 cases at steady state of 15-40years age group. Serum FA, 5-Methyl Tetrahydrofolate (5-MTHF), Dihydrofolate reductase, Interleukin-6 (IL-6), Highly sensitive C-Reactive Protein (HsCRP), and natural killer (NK) cell activity were estimated. More than 50% of the study population depicted presence of UMFA. The median UMFA level was significantly elevated in crisis group (131.8ng/mL) as compared to the steady state group (36.31ng/mL) (p = 0.041). The median value of HsCRP was significantly higher in the crisis group (18.41mg/L) than the steady state group (2.04mg/L) (p = 0.003). Similarly, IL-6 was higher in crisis group (13.29pg/mL) than steady state group (5pg/mL) (p = 0.060). The median NK cell activity was 39.28nmol/L in crisis group and 35.31nmol/L in steady state groups (p = 0.889). In bivariate correlation analysis, UMFA showed a significant negative correlation with NK cell activity (r = - 0.638; p = < 0.001) and a positive correlation with IL-6 (r = 0.571; p = 0.001) and HsCRP (r = 0.237; p = 0.200). Accumulation of UMFA affect NK cell activity, thus influence the vulnerability for crisis state. Therefore, dosage modification for FA supplementation in SCD patients is suggested.

Ferulic acid attenuated diethylnitrosamine-provoked hepato-renal damage and malfunction by suppressing oxidative stress, abating inflammation and upregulating nuclear factor erythroid related factor-2 signaling

Background Diethylnitrosamine (DEN) is a potent environmental toxin that can reach humans through the food chain. It induces proliferative, degenerative and cancerous lesions in the liver and kidneys. Objective The principal goal of the existing research was to assess the preventive impacts of ferulic acid (FA) versus DEN- provoked hepato-renal damage and malfunction. Materials and methods Adult male rats were divided into four groups: group 1 (normal control) animals orally received saline every day for 14 weeks; group 2 (DEN) animals intraperitoneally received DEN (150 mg/kg twice a week) for 2 weeks; group 3 (DEN + FA) animals were injected intraperitoneally twice a week with DEN for 2 weeks besides to oral administration of FA (100 mg/kg/day) for 14 weeks; group 4 (FA) animals were given a similar dose of FA for a similar period. Results The results revealed that FA treatment reversed the DEN-mediated elevation in serum values of the liver enzymes activities as well as urea and creatinine levels; it also augmented the hepato-renal antioxidant system that overcame DEN-induced oxidative stress deteriorations. Moreover, FA markedly reduced the DEN-induced elevated hepato-renal levels of immuno-inflammatory markers (IL-1β and TNF-α) as well as downregulated the inflammatory mediators (Bcl-2, NF-κB, and nuclear factor erythroid related factor-2 (Nrf-2)), reflecting its protective potential. Conclusion The existing results elucidate that ferulic acid could prevent and ameliorate DEN-induced hepato-renal toxicological changes and can restore livers and kidneys’ functions; this effect could be mechanized through activation of anti-inflammatory and antioxidant systems, as well as regulation of NF-κB, Bcl2, and nuclear factor erythroid related factor-2 expression.

Clinical profile of vitiligo patients and relationship with immuno-inflammatory markers

BackgroundVitiligo is the most common pigmentary disorder and is considered a chronic, cumulative, multifactorial disease. The crucial role of cytotoxic CD8+ T lymphocytes and the IFNγ/CXCL10 axis has been demonstrated in its pathogenesis. ObjectiveTo evaluate the clinical profile and immuno-inflammatory markers in patients with vitiligo in a reference medical center. MethodsCross-sectional study in which all patients with vitiligo seen at the medical center the from 2019 to 2022 were evaluated, to outline the clinical profile. Moreover, cardiovascular risk biomarkers (neutrophil/lymphocyte ratio and C-reactive protein levels) were measured, as well as cytokines and chemokines (TNFα, IFNγ, IL10, IL15 and CXCL10) in the serum of a subgroup of 30 patients. ResultsThere was a predominance of females, with a mean age of 43 years. Most were phototypes IV or V (71.3%), without comorbidities (77.55%), and without a family history of vitiligo (70.41%). Higher levels of neutrophil/lymphocyte ratio, C-reactive protein, and inflammatory cytokines/chemokines were documented in vitiligo patients when compared to the control group (non-significant). As relevant data, the highest values of CXCL10 were detected in patients with vitiligo versus controls, as well as in patients with disease of shorter duration (p<0.05). Study limitationsThe number of assessed patients was small due to recruitment difficulties caused by the COVID-19 pandemic. ConclusionThe present data contribute to confirming the relevant role of the IFNγ/CXCL10 axis in the pathogenesis of vitiligo, highlighting CXCL10 as a possible activity marker.

Circulating Inflammatory Factor Levels in the Early Phase of COVID-19 are Associated with the Progression of Respiratory Failure: A Single-Center Retrospective Study.

To evaluate the potential relationships between serum interleukin (IL)-2, IL-4, IL-6, IL-10, IL-17, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels and occurrence of respiratory failure in patients with early-stage COVID-19 disease. We analyzed clinical characteristics, laboratory parameters, and immunoinflammatory markers in 302 patients diagnosed with SARS-CoV-2 infection who required hospitalization at Changshu Hospital of Nantong University. IL-2, IL-4, IL-6, IL-10, IL-17, IFN-γ, and TNF-α levels in the peripheral blood of patients hospitalized five days after disease onset were measured using multiplex bead-based flow fluorescent immunoassay (MBFFI). Patients with respiratory failure had higher serum IL-4 [0 (0, 0.54) pg/mL], IL-6 [40.76 (12.33, 90.28) pg/mL], IL-10 [6.65 (4.12, 11.34) pg/mL], and IL-17 [9.48 (4.31, 12.13) pg/mL] levels than patients without respiratory failure (P=0.042, P<0.0001, P=0.012, and P=0.036, respectively). Serum IL-2, IFN-γ, and TNF-α levels were not significantly different between the two groups. The occurrence of respiratory failure was positively correlated with sex (R=0.122, P=0.034), lactic acid (R=0.193, P=0.007), white blood cell count (R=0.121, P=0.038), erythrocyte distribution width (R=0.131, P=0.024), thyrocalcitonin (R=0.280, P<0.0001), and D-dimer levels (R=0.214, P<0.0001) but negatively correlated with oxygen partial pressure (R=-0.208, P=0.004), oxygen saturation (R=-0.220, P=0.002), lymphocyte count (R=-0.129, P=0.026), and calcium (R=-0.152, P=0.042). Among the immunoinflammatory biomarkers, the occurrence of respiratory failure was positively correlated with IL-4 (R=-0.117, P=0.042), IL-6 (R=0.206, P<0.0001), IL-10 (R=0.145, P=0.012), and IL-17 (R=0.121, P=0.036) levels. Serum levels of pro-inflammatory cytokines IL-6 and IL-17 and anti-inflammatory cytokines IL-4 and IL-10 were significantly elevated in patients with respiratory failure and weakly positively correlated with the occurrence of respiratory failure. Further studies are required to explore these key immune mechanisms to help clinicians better manage acute complications, long-term sequelae, and possible future COVID-19 variants and be flexible in managing future epidemics and similar public health threats.

Subclinical atherosclerosis of the carotid arteries in patients with rheumatoid arthritis with low cardiovascular risk

To evaluate the detection rate of subclinical carotid atherosclerosis in rheumatoid arthritis (RA) patients with low cardiovascular risk (CVR). The study included 182 RA patients with low CVR (mSCORE<1%) and no established cardiovascular diseases and a control group comprising 100 people. Atherosclerotic lesion of the carotid arteries was assessed using Doppler ultrasound of the carotid arteries and was determined by the detection of atherosclerotic plaque (ASP) - the local increase in the thickness of the intima-media complex (IMT) >1.5 mm. Carotid ASP were observed more frequently in RA patients with low CVR than in the control group (17% versus 8%; p=0.02). The frequency of ASP in RA patients with low CVR did not depend on the disease's stage or activity and ongoing therapy. In RA, the detection of subclinical atherosclerosis was associated with traditional risk factors: carotid ASP were detected 4 times more often in men than in women (48% versus 12%, p<0.01); carotid IMT correlated with age (R=0.46), body mass index (R=0.17), LDL-C level (R=0.20), systolic blood pressure (R=0.17); p<0.05 in all cases. According to a multivariate model, in RA, the risk of developing ASP increased in the presence of dyslipidemia (odds ratio - OR 2.97; 95% confidence interval - CI 1.36-6.49; p=0.006) and arterial hypertension (OR 2.16; 95% CI 1.03-4.54; p=0.04). In RA patients with carotid ASP, sCD40L level was associated with carotid IMT (R=0.32; p=0.04) and cholesterol concentration (R=0.39; p=0.01). Subclinical atherosclerotic lesions of the carotid arteries were observed in 24% of RA patients with low cardiovascular risk and were detected almost 2 times more often than in the control group. In RA patients with low CVR, the risk of developing carotid ASP increased by 2-3 times with concomitant hypertension and dyslipidemia. The carotid IMT was associated with traditional risk factors - age, gender, lipid levels and blood pressure indicators, in cases of detection of ASP - with an immunoinflammatory marker - sCD40L.

Immuno-inflammatory markers of syntropic cardiovascular diseases

Objective: To study the immuno-inflammatory markers of coronary heart disease, arterial hypertension and their combined course. The research work included 116 patients with cardiovascular disease of middle and old age. The average age of patients is 62.4±1.27. All patients were examined at the Bukhara branch of the Republican scientific and practical Center for emergency medical care. During the analysis, it was found that the level of systolic arterial blood pressure directly depends on the concentration of fibrinogen – r = 0.30 and oppositely depends on the concentration of procalcitonin (PCT) – r = -0.3 and IL-6 – r = -0.26. At the same time, a noticeable positive association of heart rate with creatinine in the blood – r = 0.35 was also revealed. The established connections show the contribution of inflammation syndrome (immune) in the progression of hypertension, or rather, indicators of the progression of hypertension in coronary heart disease are creatinine, fibrinogen, PCT and IL-6. Due to the high and noticeable correlation with the studied immuno-biochemical parameters of blood and functional parameters of the heart, IL-6 is a more informative indicator of the progression of coronary heart disease with the risk of complications and multiple organ failure. Thus, the established connections in our studies allow us to include the conclusion that, along with the above, risk factors for the development of rupture and/ or aneurysm of the aorta in CHD are an increase in the blood level of complement C3, IL-17 and PCT. Consequently, with an increase in the level of VEGF in the blood in CHD AS, the risk of an increase in the thickness of the LV in the diastole increases, and an increase in IL-6, IL-17A and urea in the blood shows a decrease in the thickness of the LV in the diastole, which makes it possible to differentiate the restrictive variant from the hypertrophic form in atypical angina. Due to the high and noticeable correlation with the studied immuno-biochemical parameters of blood and functional parameters of the heart, IL-6 is a more informative indicator of the progression of coronary artery disease with the risk of complications and multiple organ failure.

Subclinical Carotid Atherosclerosis in Patients with Rheumatoid Arthritis at Low Cardiovascular Risk.

To evaluate the rate of subclinical carotid atherosclerosis and clinical significance of immunoinflammatory markers in patients with rheumatoid arthritis (RA) at low cardiovascular risk. The study included 275 RA patients and a control group of 100 participants without autoimmune diseases. All study participants were at low cardiovascular risk, calculated by the QRISK3 scale (<20%), and free of cardiovascular disease. Ultrasound examination of carotid arteries was performed to measure cIMT and to detect atherosclerotic plaques (ASP) in carotid arteries. sIСАМ-1, sVСАМ, and sCD40L levels were determined by enzyme immunoassay. Carotid ASP was observed more frequently in RA patients (27%) than in the control group (17%), p = 0.03. The frequency of ASP in RA patients did not depend on the disease's stage or activity. There was a significant correlation between cIMT and age, cardiovascular risk determined by QRISK3, level of total cholesterol, LDL, and blood pressure in RA patients, p < 0.05 in all cases. No correlation between cIMT and blood levels of sCD40L, sVCAM, and sICAM was found. In RA patients, a higher concentration of sVCAM was detected in the carotid ASP group compared to the non-atherosclerotic group. sCD40L was associated with cIMT and total cholesterol in the ASP group and with total cholesterol and blood pressure in non-atherosclerotic patients. Subclinical atherosclerotic lesions of the carotid arteries were observed significantly more frequently in RA patients with low cardiovascular risk than in the control group. The results of the study demonstrate the association between cIMT, traditional cardiovascular risk factors, and immunoinflammatory markers in RA patients.

Progress of peripheral blood immunoinflammatory markers in oral squamous cell carcinoma

Progress of peripheral blood immunoinflammatory markers in oral squamous cell carcinoma

Endocan: A Key Player of Cardiovascular Disease.

Endothelial dysfunction is considered to be an early change in atherosclerosis. Endocan, also known as endothelial cell specific molecule-1, is a soluble proteoglycan mainly secreted by endothelial cells. Inflammatory factors such as IL-1β and TNF-α can up regulate the expression of endocan and then affect the expression of cell adhesion molecules, such as ICAM-1 and VCAM-1, which play an important role in promoting leukocyte migration and inflammatory response. Elevated plasma levels of endocan may reflect endothelial activation and dysfunction, and is considered to be a potential immuno-inflammatory marker that may be related to cardiovascular disease. In the case of hypertension, diabetes, angina pectoris and acute myocardial infarction, the increase or decrease of serum endocan levels is of great significance. Here, we reviewed the current research on endocan, and emphasis its possible clinical value as a prognostic marker of cardiovascular disease. Endocan may be a useful biomarker for the prognosis of cardiovascular disease, but more research is needed on its mechanism of action.

Nigella sativa oil protects against cadmium-induced intestinal toxicity via promotion of anti-inflammatory mechanisms, mucin expression and microbiota integrity.

Objective:This study examined the protective effects of Nigella sativa oil (NSO) on cadmium (Cd)-induced alterations affecting gut morphology and microbiota composition, as well as the involvement of mucus glycoprotein (MUC2) and immuno-inflammatory markers (TNFα and IL-2) in the colon of rats.Materials and Methods:Male Wistar rats, randomized into four groups, were treated either with distilled water (control), CdCl2 (100 mg/kg), CdCl2+NSO (1 ml/kg) or NSO alone. After the experiments, faecal samples were processed for microbial culture on various selective media, while intestinal segments were prepared for histopathological examination and immunohistochemistry. The composition of NSO was analyzed using Gas Chromatography-Mass Spectrometry (GC-MS).Results:Oral Cd administration provoked dramatic increases in faecal counts of potentially pathogenic bacteria (Staphylococci, Enterococci, Pseudomonas and Escherichia coli), while decreasing probiotic lactobacilli counts. Cadmium treatment caused down-regulation of colonic MUC2 (p=0.003) and IL-2 (p=0.03), but increased TNFα (p=0.034), along with reduced goblet cell counts and mucus production. Conversely, treatment with NSO significantly improved Lactobacilli counts (p=0.042), while reducing the levels of potentially pathogenic species. In addition, NSO significantly restored colonic expressions of MUC2 (p=0.001), TNFα (p=0.007) and IL-2 (p=0.025) to control levels. GC-MS analysis of NSO revealed the presence of the active ingredient, thymoquinone and a high content of unsaturated fatty acids, including trans-13-octadecenoic acid and oleic acid. Conclusion:This study highlights the intestinal mucus, microbiota and immuno-inflammatory system as important protective targets of NSO against Cd-induced intestinal toxicity.

Onodera's Prognostic Nutritional Index is a novel and useful prognostic marker for gastrointestinal stromal tumors.

BACKGROUNDImmunoinflammatory markers such as the peripheral blood neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) have gained considerable attention as prognostic markers in gastrointestinal stromal tumors (GISTs). AIMTo assess the prognostic value of Onodera’s Prognostic Nutritional Index (OPNI) for GISTs.METHODSAll patients who had undergone surgical resection for a primary, localized GIST from 2009 to 2016 at our cancer center were initially and retrospectively identified. Recurrence-free survival (RFS) was calculated by the Kaplan-Meier method and compared by the log-rank test. We used multivariate Cox proportional hazard regression models to identify associations with outcome variables.RESULTSA total of 235 GISTs were identified and included for analysis under our inclusion criteria. Univariate and multivariate analyses both identified the OPNI as an independent prognostic marker, and the OPNI was associated with the primary site, tumor size, mitotic index, tumor rupture, necrosis, and modified NIH risk classification. Low OPNI (< 51.30; hazard ratio = 5.852; 95% confidence interval: 1.072–31.964; P = 0.0414) was associated with worse RFS. The 2- and 5-year RFS rates of the patients with a low OPNI were 92.83% and 76.22%, respectively, whereas 100% and 98.41% were achieved by the patients with a high OPNI.CONCLUSIONThe preoperative OPNI is a novel and useful prognostic marker for GISTs.

A View on Polymerase Chain Reaction as an Outstanding Molecular Diagnostic Technique in Periodontology.

Objectives This study presents a discussion on the fundamentals of polymerase chain reaction (PCR) and its use as a diagnostic tool in periodontology. Materials and Methods A computer-aided as well as hand-made search in PubMed and Scopus indexed journals (relevant to the topic) was done by keywords of molecular technique in periodontology, PCR, applications of PCR, and PCR in periodontics. Only the papers in the English language and outlining PCR and its association with periodontology were collected and utilized to provide a succinct review. There was no limitation for publication time. Results The results of our search showed that PCR has turned into a standard in diagnosis in the field of periodontology. A variety of researches has demonstrated that its sensitive, and specific characteristics make it a quick and effective technique of recognition, identification, and quantification of microorganisms. Identification of various immunoinflammatory markers at the mRNA expression level as well as ascertaining gene-related polymorphisms can also be performed. Conclusions The mechanisms of periodontal disease can further become clarified using PCR. Clinical Relevance. PCR as a diagnostic method can play a main part in the validation of the clinical diagnosis of periodontal disease indicating the reason, pathogenesis, clinical steps, progress, and prognosis of the disease.