Levels Of Inflammatory Biomarkers Research Articles

Can We Predict Poor Outcomes for Arthroscopic Partial Meniscectomy?: Commentary on an article by Michael R. Moore, BA, et al.: "Levels of Synovial Fluid Inflammatory Biomarkers on Day of Arthroscopic Partial Meniscectomy Predict Long-Term Outcomes and Conversion to TKA. A 10-Year Mean Follow-up Study".

Can We Predict Poor Outcomes for Arthroscopic Partial Meniscectomy?: Commentary on an article by Michael R. Moore, BA, et al.: "Levels of Synovial Fluid Inflammatory Biomarkers on Day of Arthroscopic Partial Meniscectomy Predict Long-Term Outcomes and Conversion to TKA. A 10-Year Mean Follow-up Study".

Eco-friendly Nanostructured Liquid Crystals Loaded with Clove Oil as a Sustainable Approach for Managing Infected Burn Wounds

Infections are a leading complication in patients with burns. Effective antimicrobial treatment with regenerative tissue healing is required. Utilizing components derived from plant origin such as natural oils as a sustainable and eco-friendly approach for managing disease is highly required nowadays. The aim of the current study is to assess the antibacterial and wound-healing activity of clove oil and its novel eco-friendly nanostructured liquid crystals (Eco-friendly-NLCs) formulation in treating infected burn wounds. A 23 full factorial design was used to optimize the Eco-friendly-NLCs. Clove oil and its novel nano-formulation were characterized and subjected to in vitro and in vivo assessments for their efficacy. Twenty rats were used experimentally. The optimum Eco-friendly-NLCs had 189.2 ± 1.9 nm, -22.8 ± 0.7 mV and 0.308 as values for particle size, zeta potential and polydispersity index. Transmission electron microscope images showed discrete spherical shape NLCs with no aggregations. The microbiological and pharmacological results revealed a superior efficacy regarding clove loaded Eco-friendly-NLCs in inhibiting bacterial growth (inhibition zone of 38 mm), significantly reducing inflammatory biomarker levels (p < 0.001), promoting angiogenesis and prompt wound healing. The Eco-friendly-NLCs loaded with clove oil could be considered as a promising formulation providing anti-inflammatory, anti-bacterial and wound healing effects.Graphical

Serum inflammation biomarkers level in cystoid and diffuse diabetic macular edema.

To assess serum inflammatory biomarker levels in patients with different subtypes of diabetic macular edema (DME). We retrospectively analyzed 50 eyes from 37 treatment-naïve DME patients who underwent intravitreal injection therapy between June and December 2023. Based on the morphological characteristics of macular edema in optical coherence tomography (OCT), the eyes were categorized into the cystoid macular edema (CME) group (n = 25) and diffuse retinal thickening (DRT) group (n = 25). Additionally, 25 eyes with diabetes retinopathy but without DME served as the control group. Comprehensive clinical data were reviewed, including best-corrected visual acuity (BCVA), central macular thickness (CMT), macular cube volume (VOL) and hematological examination. The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) were calculated. NLR and SII levels were significantly higher in the CME group compared to the DRT group and control group (all P < 0.01). The optimal ROC cutoff value of NLR for CME was 2.27, with 88.0% sensitivity and 68.0% specificity. The optimal ROC cutoff value of SII for CME was 447.33, with 84.0% sensitivity and 60.0% specificity. After initial intravitreal injection therapy, BCVA and VOL significantly improved in each group (all P < 0.01). However, no significant correlation was found between systemic inflammatory marker levels and postoperative changes in BCVA, CMT and VOL (all P > 0.05). Our study suggests that elevated NLR and SII levels are significantly associated with CME. Elevated serum inflammatory biomarkers may indicate a higher incidence of CME in these patients.

Association Between Left Ventricular Diastolic Dysfunction, Systemic Inflammation, and Gastrointestinal Symptoms in HIV-Positive Patients on Antiretroviral Therapy

Background/Objectives: Despite advancements in antiretroviral therapy (ART), HIV-positive individuals face heightened risks of cardiovascular and gastrointestinal (GI) complications, often linked to persistent systemic inflammation. Left ventricular diastolic dysfunction (LVDD), prevalent in HIV patients, exacerbates this inflammatory state and may contribute to worsened GI symptoms. This study aims to explore the association between LVDD, systemic inflammation, and gastrointestinal symptoms in HIV-positive patients undergoing ART. The primary objective is to analyze how LVDD contributes to the inflammatory burden and its impact on gastrointestinal health in this population. Methods: This cross-sectional study included 320 participants divided into three groups: HIV-positive with LVDD (n = 80), HIV-positive without LVDD (n = 120), and HIV-negative controls (n = 120). Levels of inflammatory biomarkers—CRP, IL-6, TNF-α, fibrinogen, IL-1β, IFN-γ, and D-dimer—were measured, and GI symptoms were assessed. Echocardiographic evaluations were performed to determine LVDD presence and severity, while multivariate logistic regression identified predictors of GI complications. Results: Patients in the HIV + LVDD group exhibited significantly elevated levels of TNF-α, CRP, and D-dimer compared to other groups, correlating with higher incidences of nausea, diarrhea, and abdominal pain. TNF-α emerged as the strongest predictor of GI symptoms, underscoring its role in the pathophysiology linking cardiovascular and GI distress in this population. Persistent inflammation and coagulation abnormalities in the ART + LVDD group suggest that ART alone may not fully mitigate these complications. Conclusions: Our findings emphasize the compounded inflammatory burden in HIV patients with LVDD, highlighting the need for integrated approaches that address both cardiovascular and GI symptoms. Anti-inflammatory therapies targeting specific biomarkers like TNF-α could improve clinical outcomes, supporting a more comprehensive strategy to managing HIV-related comorbidities beyond viral suppression.

Development and validation of predictive models of early immune effector cell-associated hematotoxicity (eIPMs).

Immune effector cell-associated hematotoxicity (ICAHT) is associated with morbidity and mortality after chimeric antigen receptor (CAR) T-cell therapy. To date, the factors associated with ICAHT are poorly characterized, and there is no validated predictive model of ICAHT specifically. Therefore, we performed comprehensive univariate analyses to identify factors associated with severe (grade 3-4) early ICAHT (eICAHT) in 691 patients who received commercial or investigational CAR T-cell therapy for hematologic malignancies. In univariate logistic regression, pre-infusion factors associated with severe eICAHT included disease type (acute lymphoblastic leukemia), pre-lymphodepletion (LD) blood counts including absolute neutrophil count (ANC), lactate dehydrogenase (LDH), and inflammatory (C-reactive protein [CRP]; ferritin, interleukin-6 [IL-6]), and coagulopathy biomarkers (D-dimer). Post-infusion laboratory markers associated with severe eICAHT included early and peak levels of inflammatory biomarkers (CRP, ferritin, IL-6), coagulopathy biomarkers (D-dimer), peak cytokine release syndrome (CRS) grade, and peak neurotoxicity grade. We trained (n = 483) and validated (n = 208) two Early ICAHT Prediction Models (eIPM): eIPMPre including pre-infusion factors only (disease type and pre-LD ANC, platelet count, LDH, and ferritin) and eIPMPost containing both pre- (disease type and pre-LD ANC, platelet count, and LDH) and post-infusion (day +3 ferritin) factors. Both models generated calibrated predictions and high discrimination (area under the receiver operating characteristic curve [AUROC] in test set: 0.87 for eIPMPre and 0.88 for eIPMPost), with higher net benefit in decision curve analysis for eIPMPost. Individualized predictions of severe eICAHT can be generated from both eIPMs utilizing our online tool (available at https://eipm.fredhutch.org).

State-specific GluCEST alterations in insular subregions are associated with depression and plasma inflammatory biomarker levels in patients with inflammatory bowel disease

BackgroundDepression commonly co-occurs with inflammatory bowel disease (IBD). Abnormal glutamate levels in the insula and altered plasma inflammatory biomarkers are observed in IBD and depression. However, the changes in glutamate concentrations in insular subregions in IBD and their relationship with depression and inflammatory markers remain unclear. This study aimed to investigate differences in glutamate concentrations in insular subregions between IBD patients and healthy controls (HCs) and their correlation with depression scores and inflammatory markers. MethodsForty-two IBD patients (19 active, IBD-A; 23 in remission, IBD-R) and 46 HCs underwent glutamate chemical exchange saturation transfer (GluCEST) magnetic resonance imaging. Blood samples from 37 IBD patients were collected for plasma inflammatory biomarker analysis. GluCEST indices in insular subregions were measured. The Hospital Anxiety and Depression Scale (HADS-D) was used to estimate depression symptoms. Whole-brain voxel-based analysis using one-way ANOVA explored between-group differences in GluCEST indices within the insula. FDR-corrected partial correlation analysis evaluated the relationships between GluCEST, depression symptoms, and inflammatory factors. ResultsGluCEST indices decreased in IBD patients in the left dorsal dysgranular subregion of the insula (dId) (uncorrected p < 0.001, cluster-level FWE-corrected p < 0.05). GluCEST indices in the left dId showed a significant positive correlation with HADS-D in IBD-R (FDR corrected q < 0.05). Additionally, GluCEST indices in the left dId were negatively correlated with CXCL9 (FDR corrected q < 0.05). ConclusionState-specific GluCEST alterations in the left dId are a cerebral metabolic feature of IBD. These changes are associated with depression and inflammatory biomarkers, suggesting that the brain-immune-gut axis might underlie depression in IBD patients.

Genetic Evidence of Obesity-Induced Chronic Wounds Mediated by Inflammatory Biomarkers.

Background: Obese patients are increasingly recognized as being at higher risk for skin diseases, particularly chronic wounds. While the exact mechanisms remain unclear, obesity is suspected to influence the development of chronic injuries via inflammatory biomarkers. Single nucleotide polymorphisms (SNPs) may further influence gene expression, protein function, and levels of inflammatory biomarkers through various mechanisms, thereby modulating inflammatory responses that contribute to wound pathogenesis. Methods: A two-sample two-step Mendelian Randomization (MR) was employed to explore the causal relationship between obesity and chronic wounds, focusing on the mediating role of inflammatory biomarkers. SNPs were used as instrumental variables (IVs) to infer causality. Obesity-related genetic data were sourced from the UK Biobank and GIANT consortium. Genome-wide association studies provided data on 92 inflammatory biomarkers, involving 14,824 and 575,531 individuals. Pressure injuries, lower limb venous ulcers, and diabetic foot ulcer data were obtained from FinnGen R10 and the Pan-UK Biobank. Results: Obesity significantly increased the risk of pressure injuries, lower limb venous ulcers, and diabetic foot ulcers. CCL19, hGDNF, IL-12B, and TNFRSF9 were identified as mediators in obesity-induced lower limb venous ulcers. Conclusion: This study provides genetic evidence that obesity leads to lower limb venous ulcers via inflammatory biomarkers, suggesting potential therapeutic targets for intervention.

Effect of omalizumab on inflammatory markers in COVID-19: an exploratory analysis of the COVID-19 immunologic antiviral therapy with omalizumab (CIAO) trial.

The CIAO trial recently demonstrated a probable clinical benefit of omalizumab in the treatment of severe COVID-19; however, the mechanism underlying this benefit remains unclear. Therefore, we sought to longitudinally assess the impact of omalizumab on serum cytokines in CIAO trial patients to determine its mechanism of action. Blood samples were collected on days 0, 2, 7, and 14 from patients recruited into the CIAO trial and who consented to this substudy. Blood samples were tested by a panel of 25 inflammatory cytokines, as well as for markers of mast cell activation. Levels of inflammatory biomarkers were compared over time between omalizumab- and placebo-treated patients by generalized linear mixed-effects model. Associations between biomarkers and clinical outcomes were investigated by mixed-effects logistic regression. Nineteen patients were recruited into this substudy; 10 were assigned to placebo and 9 to omalizumab. Monokine induced by gamma interferon was significantly positively associated with severe COVID-19 (Odds Ratio [OR] = 1.06, 95%CI = 1.00-1.11, p = 0.043). Further, omalizumab significantly reduced interleukin-15 (Coefficient = -0.95, p = 0.048) and macrophage inflammatory protein-1 (Coefficient = -1.31, p = 0.010) levels. However, neither was significant in analyses adjusting for multiple hypothesis testing. Although limited by a small sample size, these results suggest that omalizumab's potential benefit in COVID-19 may be mediated independently of modulation of the measured serum biomarkers. Further studies are needed to investigate omalizumab's mechanism of action in COVID-19.

Is there an association between inflammatory biomarkers and organ space surgical site infection after emergency laparotomy in massively transfused trauma patients?

BackgroundThe relationship between inflammatory biomarkers (IB) and organ space surgical site infections (OS-SSIs) after emergency laparotomy (EL) is poorly understood. MethodsRetrospective, single-center analysis of patients in the Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) trial who underwent EL and survived 48 ​h after admission was performed. IB levels of IL-6, IL-8, G-CSF, MCP-1, neutrophil to lymphocyte ratio, and platelet to lymphocyte ratio were analyzed. IB and OS-SSIs association was evaluated using the Wilcoxon rank sum test. ResultsOf 74 eligible patients, 80 ​% were male, 69 ​% sustained blunt trauma, the injury severity score was 31 (24–41), and 22 ​% developed OS-SSIs. Levels of IL-6 (12, 24 ​h), IL-8 (2, 12, 24, 72 ​h), and MCP-1 (24 ​h) were higher in OS-SSI patients (P ​< ​0.05). ConclusionsIL-6, IL-8, and MCP-1 levels were associated with OS-SSIs in PROPPR patients who underwent EL. The IB may help to predict high-risk patients for OS-SSIs.

Inflammation-attenuating effect of carbon dioxide versus room-air environment in a rat laparotomy model.

The mechanism by which laparoscopic operations induce lower post-operative inflammatory response compared to open surgery was investigated with regard to the effect of the type of gas environment. Rats were subjected to midline laparotomy at either CO2 (group CO2) or room-air environment (group Air) or to anesthesia only (group Control) under atmospheric pressure conditions. At various timepoints after surgery (1, 3, 6, 24, or 48h), the expression of inflammation biomarkers interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), and nuclear factor-κΒ (NFκΒ) were assessed immunohistochemically in tissue samples excised from the liver, intestine, and kidneys, accompanied by histopathologic analysis, and their levels were measured by ELISA in blood samples. Tissue expression of IL-6, TNFα, and NFκΒ was downregulated in the liver and intestine in group CO2 compared to group Air and in the kidneys in group Air compared to group CO2. However, no differences were noted among groups regarding the histopathologic score of organ tissues and the blood serum levels of inflammation biomarkers. Post-operative local inflammatory response was lower in intra-peritoneal organs of rats subjected to laparotomy at CO2 rather than room-air environment under atmospheric pressure conditions.

Endodontic treatment modifies circulatory inflammatory mediator levels: A systematic review with meta-analysis.

There is limited and conflicting data on the reduction of circulatory inflammatory mediators in patients with apical periodontitis (AP) following endodontic treatment. To answer the following research question: in adult healthy patients with AP [Population (P)], is there a difference before [Comparator (C)] and after various endodontic treatments (nonsurgical, surgical or retreatment) [Intervention (I)] on systemic levels of inflammatory biomarkers [Outcome (O)] in the follow-up period[Time (T)]? An electronic literature search was conducted in the databases Scopus, PubMed, Clarivate Analytics' Web of Science, Cochrane Database of Systematic Reviews and Grey literature from inception to July 2024 with no language restrictions. Observational studies examining changes in serum levels of inflammatory mediators were included. Two independent reviewers selected studies, extracted data and critically appraised the included studies. Qualitative and quantitative (meta-analysis) data synthesis methods were employed. The Newcastle-Ottawa Scale was used to assess the quality of the included studies. Sixteen studies met the inclusion criteria, of which six were included in the meta-analysis. These studies were published between 1992 and 2024, involving a total of 596 patients (54% females) aged between 16 and 75 years. The meta-analysis of pooled data showed a significant decrease in high-sensitive C-reactive protein (hs-CRP) levels in the serum of patients with AP 6 months after treatment [2.26 ± 1.76 versus 1.28 ± 1.06 mg/L, (Z = 2.03, p = .04)] and a decrease in interleukin-1β (IL-1β) levels 12 months after treatment [13.01 ± 5.95 versus 10.86 ± 3.52 pg/mL, (Z = 3.72, p < .01)]. One study was assessed as poor quality, while all others were considered high quality. Despite the differences in methodologies across the included studies, it has been established that effective endodontic treatment leads to a reduction in systemic inflammatory biomarkers in the body. Following effective endodontic treatment in patients with AP, the systemic levels of hs-CRP and IL-1β exhibit a significant reduction at 6 and 12 months, respectively. Further clinical studies should investigate whether effective endodontic treatment and reduced levels of investigated biomarkers may change the clinical presentation of systemic diseases. PROSPERO database (CRD42024559271).

Abstract 4144530: IL-37 promotes resolution of Right Heart Disease-induced inflammation and atrial fibrillation.

INTRODUCTION: Atrial Fibrillation (AF) is the most common cardiac arrhythmia. Hypertension, obesity, diabetes or right heart disease (RHD) are important risk factors for AF. Inflammation stands as a common denominator among most AF risk factors. Studies have shown that patients with AF present high levels of circulating IL-18. Our group recently described that inflammation-resolution may prevent AF in RHD, however, the mechanism remains unclear. To inhibit IL-18-induced inflammation, IL37, a specific antagonist of IL-18-receptor was shown to attenuate cardiac fibrosis in a mice model of myocardial infarction, but little is known about its efficacy to prevent AF. HYPOTHESIS: IL-37 curbs RHD-induced atrial inflammation and AF vulnerability. METHODS: To induce right-sided cardiac hypertrophy and dilation, pulmonary artery banding (PAB) was performed in male and female Wistar rats (250-300g). Sham animals did not receive the ligation. Animals were randomized into four groups: Sham and PAB treated or not with IL37 (100 ng/ml/kg). Electrophysiological studies and echocardiography were performed in vivo before sacrifices at day (D)0, D7, D14 and D21. To analyze the atrial conduction, right atrial (RA) optical mapping was performed on Langendorff-perfused hearts. Histology, western blot, and qPCR were performed to study the expression of proteins and genes involved in atrial inflammation, fibrosis, and electrical remodeling. RESULTS: Twenty-one days after surgery, PAB rats were more vulnerable to AF and developed severe right-sided hypertrophy and dilation compared to Sham. Reliable to clinical evidence, female rats might be more resistant to AF than males. AF was associated with increased RA levels of inflammatory biomarkers including IL18, IL1β, and IL6. IL37 treatment was associated with decreased atrial expression of inflammatory markers. CONCLUSION: IL37 is a potential new therapeutic strategy to reduce atrial inflammation and prevent AF vulnerability in RHD.

The Prevalence of Malnutrition and Sarcopenia and the Relationship with Inflammation and Anemia Among Community-Dwelling Older Adults: A Preliminary Cross-Sectional Study.

Background: Older people are more likely to have poor nutrition and low muscle mass, which leads to poor physical performance and anemia, resulting in a poor quality of life and risks to mobility and mortality. Furthermore, malnutrition may, in part, raise the level of inflammatory biomarkers as well as muscle catabolism. Moreover, a range of indices related to systemic inflammation, obtained from routine complete blood count (CBC) tests, have been applied to inflammation markers. However, these biomarkers remain insufficiently addressed in the evidence supporting the presence of sarcopenia and malnutrition. This study aimed to explore sarcopenia in terms of malnutrition, anemia, and inflammation among Thai community-dwelling older people. Methods: This study enrolled community-dwelling older people aged 60 years and above. All participants were requested to complete a questionnaire assessing for sarcopenia (SARC-F) and nutritional status using the mini nutritional assessment (MNA). In addition, blood samples were obtained for the CBC test. Logistic regression analysis explored the risk of sarcopenia, CBC, and malnutrition status. Results: Of 126 older people (aged 62-88 years) enrolled, 12 individuals (9.52%) had sarcopenia. Furthermore, 34.9% and 5.56% of the participants were demonstrated to have anemia and malnutrition, respectively. Nutrition status was positively associated with hemoglobin levels (r = 0.241, p = 0.007) and negatively related to SARC-F scores (r = -0.190, p = 0.034). Older people with anemia show an increased risk of malnutrition at an odds ratio (OR) of 3.375. Moreover, individuals with anemia were at a higher risk of developing sarcopenia (OR 4.982) than those with no anemia. However, individuals with a high level of inflammatory markers, e.g., a high systemic inflammatory response index (SIRI) and monocyte-to-lymphocyte ratio (MLR), had a higher risk of sarcopenia than those with low SIRI and MLR values. The systemic immune-inflammation index (SII) and platelet-to-lymphocyte ratio (PLR) were also positively associated with SARC-F scores. Conclusions: The association between sarcopenia, malnutrition status, and anemia might overlap in clinical manifestation. In addition, future research directions regarding the utility of routine CBC testing should focus on sarcopenia and malnutrition status.

Noninvasive, Multimodal Inflammatory Biomarker Discovery for Systemic Inflammation (NOVA Study): Protocol for a Cross-Sectional Study.

Prolonged systemic inflammation is recognized as a major contributor to the development of various chronic inflammatory diseases. Daily measurements of inflammatory biomarkers can significantly improve disease monitoring of systemic inflammation, thus contributing to reducing the burden on patients and the health care system. There exists, however, no scalable, cost-efficient, and noninvasive biomarker for remote assessment of systemic inflammation. To this end, we propose a novel, multimodal, and noninvasive approach for measuring inflammatory biomarkers. This study aimed to evaluate the relationship between the levels of inflammatory biomarkers in serum (gold standard) and those measured noninvasively in urine, sweat, saliva, exhaled breath, stool, and core body temperature in patients with systemic inflammation. This study is a single-center, cross-sectional study and includes a total of 20 participants (10 patients with systemic inflammation and 10 control patients). Eligible participants provide serum, urine, sweat, saliva, exhaled breath, and stool samples for biomarker analyses. Core body temperature is measured using a sensor. The primary end point is the level of C-reactive protein (CRP). The secondary end points are interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor-α levels. The tertiary end points are fractional exhaled nitric oxide, calprotectin, and core body temperature. Samples will be collected in 2 batches, enabling preliminary analysis of the first batch (patients 1-5 from each group). The full analysis will include both batches. CRP and cytokine levels will be measured using enzyme-linked immunosorbent assay and electrochemiluminescence immunoassay. For statistical analysis, the Shapiro-Wilk test will be used to evaluate the normality of the distribution in each variable. We will perform the 2-tailed t test or Wilcoxon rank sum test to compare the levels of inflammatory biomarkers between patients with systemic inflammations and control patients. Pearson and Spearman correlation coefficients will assess the relationship between inflammatory biomarkers from noninvasive methods and serum biomarkers. Using all-subset regression analysis, we will determine the combination of noninvasive methods yielding the highest predictive accuracy for serum CRP levels. Participants' preferences for sampling methods will be assessed through a questionnaire. The study received ethics approval from the independent research ethics committee of Canton Zurich on October 28, 2022. A total of 20 participants participated in the study measurements. Data collection started on February 22, 2023, and was completed on September 22, 2023. Participants were on average 52.8 (SD 14.4; range 24-82) years of age, and 70% (14/20) of them were women. The analysis results reporting findings are expected to be published in 2025. This study aims to evaluate the feasibility of noninvasive, multimodal assessment of inflammatory biomarkers in patients with systemic inflammation. Promising results could lead to the creation of noninvasive and potentially digital biomarkers for systemic inflammation, enabling continuous monitoring and early diagnosis of inflammatory activity in a remote setting. DERR1-10.2196/62877.

Relationship between Diet-Related Inflammation and Hospitalization Risk and Disease Severity in Patients with COVID-19

Background: Increased serum concentrations of inflammatory biomarkers in patients indicate a strong association between COVID-19 and inflammation. However, the association between diet-related inflammation and COVID-19 has been less investigated. The aim of this study is to investigate whether the inflammatory scores of the diet are associated with the severity of COVID-19 disease and the probability of hospitalization of patients. Methods: The authors conducted a cross-sectional study involving 141 patients with COVID-19. The empirical dietary inflammatory pattern (EDIP) and dietary inflammation scores (DIS) were calculated based on a 147-item semi-quantitative food frequency questionnaire. The association between serum levels of inflammatory biomarkers and diet-related inflammation was also investigated. Results: 74 inpatients and 87 outpatients participated in this study. Higher DIS scores were significantly associated with an increased risk of COVID-related hospitalization (Tertile3 vs. tertile1: OR = 3·62; 95 % CI 1·43 to 9·14, P=0·008 after fully adjustment). This association with EDIP was also observed, but it was not significant. Conclusion: The data from this provide evidence that a pro-inflammatory diet was associated with higher risk of hospitalization due to high severity of COVID-19.

Cardioprotective potential of sakuranetin to counteract polyethylene microplastics induced cardiotoxicity

Polyethylene microplastics (PEMPs) are toxic environmental contaminants which can impair multiple organs including heart. Sakuranetin (SKN) is a potential flavonoid with diverse pharmacological benefits. This research was undertaken to analyze the defensive impact of SKN to avert PEMPs-induced cardiotoxicity. Rats were allocated into 4 separate groups: control, PEMPs (1.5 mg kg−1), PEMPs + SKN (1.5 mg kg−1 + 10 mg kg−1) & only SKN (10 mg kg−1) treated group. After 30 days of treatment, our results revealed that PEMPs exposure reduced Nrf2 & antioxidant genes whereas increased Keap1 expression. Besides PEMPs intoxication escalated the level of cardiac biomarkers (CPK, LDH, Troponin I & CK-MB). Additionally, it lessened the activities of GSH, GST, SOD, HO-1, CAT, GSR, GPx whereas the levels of MDA and OS were increased. Conversely, the levels of inflammatory biomarkers i.e., COX-2 activity IL-1β, TNF-α, NF-kB & IL-6 were augmented. Besides, the expressions of apoptotic biomarkers i.e., Bax & caspase-3 were enhanced while the Bcl-2 expression was decreased. Furthermore, histological analysis indicated substantial cardiac tissue damage. However, SKN treatment significantly restored the PEMPs-induced biochemical as well as histological impairments. Therefore, SKN could be used as a therapeutic compound to ameliorate PEMPs-induced cardiac impairments in rats, possibly due to its tremendous pharmacotherapeutic potential.

Inflammatory biomarker analysis confirms reduced disease severity in heterozygous patients with familial Mediterranean fever

IntroductionFamilial Mediterranean fever (FMF) is a genetic disease leading to recurrent episodes of inflammation. Two pathogenic variants are required for classical disease, but the disease can occur in heterozygous patients....

Short-Term Changes in TNF-Alpha, IL-6 and Adiponectin Following Bariatric Surgery in Caucasian Obese Adults: An Observational Case-Control Study.

Background and Objectives: Overweight and obesity are well-known conditions that negatively impact the health and lifestyle of an individual. Bariatric surgery is one of the most efficient weight loss techniques. Besides the main effect on the bodyweight, improvement in the levels of inflammatory biomarkers, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalfa), and others, has been observed. The purpose of this study was to establish the correlations between obesity-linked chronic systemic inflammation (estimated with inflammatory cytokine levels) and the weight loss process after metabolic surgery. Materials and Methods: An observational cohort study included two categories: the patients with obesity-bariatric group and the patients without obesity-control group. The study was performed between 1 February 2021 and 1 March 2023. Baseline characteristics, anthropometrics, biochemical assessment and inflammatory biomarkers were measured both before surgery and one year after the procedure, in the case of the bariatric group. The control group was assessed in the same period as the pre-surgery bariatric group. The bariatric group underwent two types of bariatric procedures: the majority underwent laparoscopic sleeve gastrectomy whereas a select few underwent one anastomosis laparoscopic gastric bypass. Results: We performed a prospective study comprising 55 Caucasian patients-from which 33 patients had morbid obesity, a mean age of 41.76 ± 10.78 and a mean BMI of 43.34± 7.51 kg/m2. The preoperative levels of IL-6 were positively correlated with waist circumference (r = 0.354, p = 0.043), weight (r = 0.549, p = 0.001) and BMI (r = 0.520, p = 0.002). After applying the Kruskal-Wallis test and Dunn's test, significant differences for IL-6 (p = 0.010) and adiponectin (p = 0.024) were obtained for values recorded pre- and post-surgery. No correlation was found between adiponectin, IL-6, TNF- α levels and anthropometric indices after surgery. Our study showed that bariatric surgery significantly changes the values of inflammatory cytokines one year after surgery. Nevertheless, we did not find significant correlations between the baseline values of these inflammatory markers and the weight loss process after surgery at a short-term (one-year) follow-up. Conclusions: Our study demonstrated that bariatric surgery significantly changes the level of inflammatory cytokines one year after operation. We demonstrate that preoperative levels of IL-6 are positively correlated with age, WC, and BMI.

Extra virgin olive oil beneficial effects on memory, synaptic function, and neuroinflammation in a mouse model of Down syndrome.

Clinical and preclinical studies have shown that extra virgin olive oil (EVOO), a major component of the Mediterranean diet, has beneficial effects on brain aging and cognition. Individuals with Down syndrome develop age-dependent cognitive decline and synaptic dysfunction. However, whether EVOO intake is beneficial in Down syndrome is not known. In this study, by implementing a mouse model of Down syndrome, we aimed to investigate the effect that chronic administration of EVOO has on memory, synaptic function, and neuroinflammation. Starting at 4 months of age Ts65dn mice were randomized to receive EVOO for 5 months in their diet, after which they were tested for learning and memory impairment. After euthanasia, synaptic function was measured in freshly obtained hippocampal slices, whereas brain tissues were assessed for inflammatory biomarkers. Compared with controls, mice receiving EVOO had a significant improvement in learning and spatial memory. Additionally, field potential recordings showed that treated mice had an improvement in synaptic function. Finally, array analysis showed that EVOO modulated the expression levels of several inflammatory biomarkers. Chronic administration of EVOO to a mouse model of Down syndrome has beneficial effects on memory impairments, synaptic function deficits and neuroinflammation. Our findings provide additional support for the potential therapeutic effects of EVOO also in individuals with Down syndrome.

Increased circulating levels of standardized inflammatory and endothelial dysfunction biomarkers in patients with myocardial infarction with nonobstructive coronary arteries

Abstract Introduction Around 10% of patients with acute myocardial infarction (AMI) present with nonobstructive coronary arteries (MINOCA), for which the underlying pathophysiology is often uncertain. Our aim was to evaluate inflammatory burden and endothelial dysfunction in MINOCA patients by assessing biomarkers in both acute and stable phases. Methods An analytical and observational study at a University Hospital involving 166 MI patients admitted over the past 3years. Following ESC guidelines, patients were categorized into MINOCA or myocardial infarction with significant coronary artery disease (MI-CAD) groups. Circulating levels of inflammatory biomarkers (interleukin-6(IL-6), tumor necrosis factor-α(TNF-α) and high-sensitivity C-reactive protein(hs-CRP)) and of endothelial dysfunction (asymmetric dimethylarginine (ADMA)) were measured in 44 MINOCA patients and 122 MI-CAD patients at acute phase (admission and discharge) and stable phase (2months after MI). As biomarker levels may vary with MI size, each value was standardized by dividing it by the peak troponin, resulting in a biomarker/troponinT ratio. We evaluated the effects of standardized (SB) and non-standardized (NSB) biomarker values using a multivariate regression model adjusted for age and sex. Results We analyzed 166 patients (median age:68 years, 70% males). MI-CAD patients had higher peak high-sensitive troponinT (hs-TnT) levels upon admission compared to those with MINOCA (1491ng/L vs 247ng/L,p&amp;lt;0.001),likely due to larger infarctions generating higher levels of inflammation. When examining the association between infarct size, as measured by peak hs-TnT values, and biomarker levels, we observed a significant dose-response relationship for hs-CRP at admission (βcoefficient 0.16 [95%CI,0.02-0.29],p0.02) and IL-6 at admission (βcoefficient 0.15 [95%CI,0.04-0.27],p0.01). Significant positive associations were found between MINOCA and all SBs, both during the acute phase and in follow-up. During the acute phase ORs ranged from 1.35to2.7 (p&amp;lt;0.05) for inflammatory biomarkers and from 2.34 to 2.76 (p&amp;lt;0.01) for ADMA. In the stable phase ORs ranged from 1.49to3.06 (p&amp;lt;0.05) for inflammatory biomarkers, and OR was 2.79(p&amp;lt;0.01) for ADMA (Figure 1). In contrast, none of the NSBs were associated with MINOCA. Regarding temporal biomarker changes, during the acute phase of MI and 2 months post-event, both MINOCA and MI-CAD patients showed similar trends. However, MINOCA patients consistently maintained elevated inflammatory activity and ADMA concentrations only when biomarkers were standardized by infarct size (Figure 2). Conclusions Higher levels of SBs were consistently associated with MINOCA, both during the acute phase of the event and in follow-up, compared to MI-CAD. Consequently, this study suggests that the inflammatory burden, measured by heightened levels of standardized inflammatory biomarkers, and endothelial dysfunction, as measured by ADMA, may play a role in the pathophysiology of MINOCA.Boxplots for SBs at three time points.Temporal changes in biomarker levels.