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Due to the lack of effective treatments, osteoarthritis (OA) remains a challenge for clinicians. Quercetin, a bioflavonoid, has shown potent anti‐inflammatory effects. However, its effect on preventing OA progression and the underlying mechanisms are still unclear. In this study, Sprague–Dawley male rats were divided into five groups: control group, OA group (monosodium iodoacetate intra‐articular injection), and three quercetin‐treated groups. Quercetin‐treated groups were treated with intragastric quercetin once a day for 28 days. Gross observation and histopathological analysis showed cartilage degradation and matrix loss in the OA group. High‐dose quercetin‐group joints showed failure in OA progression. High‐dose quercetin inhibited the OA‐induced expression of MMP‐3, MMP‐13, ADAMTS4, and ADAMTS5 and promoted the OA‐reduced expression of aggrecan and collagen II. Levels of most inflammatory cytokines and growth factors tested in synovial fluid and serum were upregulated in the OA group and these increases were reversed by high‐dose quercetin. Similarly, subchondral trabecular bone was degraded in the OA group and this effect was reversed in the high‐dose quercetin group. Our findings indicate that quercetin has a protective effect against OA development and progression possibly via maintaining the inflammatory cascade homeostasis. Therefore, quercetin could be a potential therapeutic agent to prevent OA progression in risk groups.

L-carnitine supplementation may be beneficial in improving inflammatory conditions and reducing the level of inflammatory cytokines. Therefore, according to the finding of randomized controlled trials (RCTs), the systematic review and meta-analysis aimed to investigate the effect of L-carnitine supplementation on inflammation in adults. To obtain acceptable articles up to October 2022, a thorough search was conducted in databases including PubMed, ISI Web of Science, the Cochrane Library, and Scopus. A random-effects model was used to estimate the weighted mean difference (WMD). We included the 48 RCTs ( n  = 3255) with 51 effect sizes in this study. L-carnitine supplementation had a significant effect on C-reactive protein (CRP) ( p <  0.001), interleukin-6 (IL-6) ( p =  0.001), tumor necrosis factor-α (TNF-α) ( p =  0.002), malondialdehyde (MDA) ( p =  0.001), total antioxidant capacity (TAC) ( p =  0.029), alanine transaminase (ALT) ( p <  0.001), and aspartate transaminase (AST) ( p <  0.001) in intervention, compared to the placebo group. Subgroup analyses showed that L-carnitine supplementation had a lowering effect on CRP and TNF-α in trial duration ≥ 12 weeks in type 2 diabetes and BMI ≥ 25 kg/m 2 . L-carnitine supplementation reduced ALT levels in overweight and normal BMI subjects at any trial dose and trial duration ≥ 12 weeks and reduced AST levels in overweight subjects and trial dose ≥ 2 g/day. This meta-analysis revealed that L-carnitine supplementation effectively reduces the inflammatory state by increasing the level of TAC and decreasing the levels of CRP, IL-6, TNF-α and MDA in the serum.

Retinitis pigmentosa (RP) is characterized by progressive loss of vision due to photoreceptor degeneration leading to secondary inflammation. The urokinase‐type plasminogen activator (uPA) system contributes to retinal inflammation, but its role in RP is unknown. In the rd10 mouse model of RP, we addressed this question with the use of the peptide UPARANT designed to interact with the uPA system. UPARANT was systemically administered from post‐natal day (PD) 10 to PD30 when its efficacy in RP rescue was investigated using electroretinographic recordings, Western blot and immunocytochemistry. Temporal profile of protein expression in the uPA system was also investigated. UPARANT reduced both Müller cell gliosis and up‐regulated levels of inflammatory markers and exerted major anti‐apoptotic effects without influencing the autophagy cascade. Rescue from retinal cell degeneration was accompanied by improved retinal function. No scotopic phototransduction was rescued in the UPARANT‐treated animals as determined by the kinetic analysis of rod‐mediated a‐waves and confirmed by rod photoreceptor markers. In contrast, the cone photopic b‐wave was recovered and its rescue was confirmed in the whole mounts using cone arrestin antibody. Investigation of the uPA system regulation over RP progression revealed extremely low levels of uPA and its receptor uPAR both of which were recovered by HIF‐1α stabilization indicating that HIF‐1 regulates the expression of the uPA/uPAR gene in the retina. Ameliorative effects of UPARANT were likely to occur through an inhibitory action on up‐regulated activity of the αvβ3 integrin/Rac1 pathway that was suggested as a novel target for the development of therapeutic approaches against RP.

This study examines the distribution characteristics of pathogenic bacteria in respiratory infections and their relationship with inflammatory markers to guide clinical drug use. We selected 120 patients with lower respiratory tract infection in the electronic medical record system of Xinjiang Provincial People's Hospital from March 2019 to March 2023 for a case-control study. Using Indirect Immunofluorescence Antibody test(IFA), blood routine, C-reactive Protein (CRP), and High-sensitivity C-reactive Protein(hsCRP), we detected nine respiratory pathogens (Respiratory syncytial virus; Influenza A virus; Influenza B virus; Parainfluenza virus; Adenovirus; Mycoplasma pneumoniae; Chlamydia pneumoniae; Legionella pneumophila type 1; Rickettsia Q) in all patients and analyzed their distribution and correlation. The patients were divided into three groups [Respiratory Syncytial Virus Immunoglobulin M(RSV-IgM) positive group A, Mycoplasma Immunoglobulin M(MP - IgM) positive group B, antibody - negative group with elevated hsCRP, 40 patients each]. We compared differences in hsCRP, platelet count, White Blood Cells(WBC), and Neutrophil(NE) among the groups. We conducted a systematic sorting and analysis of variables exhibiting significant differences. The results of the multivariate logistic regression analysis indicated that inflammatory markers, including white blood cell count (WBC) (OR 3.85, 95% CI: 1.116-1.623), neutrophils (NE) (OR 2.26, 95% CI: 1.091-1.312), high-sensitivity C-reactive protein (HsCRP) (OR 1.95, 95% CI: 1.068-14.640), lymphocytes (OR 1.30, 95% CI: 1.045-1.134), platelet count (OR 1.34, 95% CI: 1.625-2.760), and C-reactive protein (CRP) (OR 3.80, 95% CI: 1.232-2.379), were significantly associated with the presence of pathogenic bacteria. There was significant correlation between inflammatory markers and pathogenic bacteria in patients with lower respiratory tract infection in Xinjiang region.

Background: We tested the hypothesis that nebulized budesonide would improve lung mechanics and oxygenation in patients with early acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) during protective mechanical ventilation strategy without adversely affecting systemic hemodynamics. Methods: Patients with ALI/ARDS were included and assigned into two groups; budesonide group (30 cases) in whom 1 mg-2 ml budesonide suspension was nebulized through the endotracheal tube and control group (30 cases) in whom 2 ml saline (placebo) were nebulized instead of budesonide. This regimen was repeated every 12 h for three successive days alongside with constant ventilator settings in both groups. Hemodynamics, airway pressures, and PaO2/FiO2were measured throughout the study period (72 h) with either nebulized budesonide or saline. Furthermore, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) were analyzed serologically as markers of inflammation at pre- and post-nebulization sessions. Results: We found a significant difference between the two groups regarding PaO2/FiO2 (P = 0.023), peak (P = 0.021), and plateau (P = 0.032) airway pressures. Furthermore, TNF-α, IL-1β, and IL-6 were significantly reduced after budesonide nebulizations. No significant difference was found between the two groups regarding hemodynamic variables. Conclusion: Nebulized budesonide improved oxygenation, peak, and plateau airway pressures and significantly reduced inflammatory markers (TNF-α, IL-1β and IL-6) without affecting hemodynamics. Trial Registry: Australian New Zealand Clinical Trial Registry (ANZCTR) at the number: ACTRN12615000373572.

Background Studies have shown that cytokines play a role in bone remodeling. Methods In 1993, all hospital births occurred in Pelotas (Brazil) were identified and a total of 5249 newborns were included in the present cohort. Sub-samples of this cohort were visited during childhood and all members were traced at 11, 15, 18 and 22 years old. At 18 and 22 years the following biomarkers were measured: IL-6, CRP and adiponectin (the last one in a sub-sample) and bone mineral density (BMD-mg/cm 2 ) was evaluated at 22 years. Crude regression analysis as well as adjusted for confounders (birth weight, pregnancy maternal smoking, gestational age, skin color, schooling, income, smoking, alcohol, physical activity, medical diagnosis of asthma, diabetes and hypertension, BMI, height, calcium intake, corticosteroid use, age at menarche, insulin and testosterone) were performed between the three biomarkers and the whole-body, lumbar spine and femoral BMD. Results No statistical significant association was found between IL-6 and CRP with BMD, in males. Significant inverse association in the adjusted analysis, among females, was found for the highest tertiles of CRP at 22 y (beta − 15.2 mg/cm 2 ; 95% CI: -25.4; − 4.9; p  = 004), of CRP and IL-6 at 22 years (beta − 20.0 mg/cm 2 ; 95% CI: -31.7; − 8.3; p  = 0.003), and of IL-6 and CRP at both ages (beta − 20.3 mg/cm 2 ; 95% CI: -38.0; − 2.5; p  = 0.001) with total body BMD. Significant association, among males, was also found between the highest tertile of adiponectin at 22 y (beta − 23.3 mg/cm 2 ; 95% CI: -35.5; − 11.1; p  = < 001; beta − 22.5 mg/cm 2 ; 95% CI: -42.9; − 2.2; p  = 0.03; and beta − 31.8 mg/cm 2 ; 95% CI: -55.5; − 9.1; p  = 0.006) and total body, lumbar spine and femur neck BMD, respectively; and, among females, − 17.8 mg/cm 2 ; 95% CI: -34.9; − 0.9; p  = 0.033, with lumbar spine BMD. Conclusion CRP at 22 years, in females, seems to be a marker for total body BMD; adiponectin at 22 years is also a marker for BMD at the three sites, in males, and for lumbar spine BMD, in females.

The mechanisms whereby regular exercise reduces chronic inflammation remain unclear. We investigated whether regular aerobic exercise alters basal levels of interleukin (IL)‐10 and IL‐4 in two randomized trials of physical activity. The Alberta Physical Activity and Breast Cancer Prevention Trial (ALPHA, n = 320) and the Breast Cancer and Exercise Trial in Alberta (BETA, n = 400) were two‐center, two‐armed randomized trials in inactive, healthy, postmenopausal women. Both trials included an exercise intervention prescribed five times/week and no dietary changes. In ALPHA, the exercise group was prescribed 225 min/week versus no activity in the controls. BETA examined dose‐response effects comparing 300 (HIGH) versus 150 (MODERATE) min/week. Plasma concentrations of IL‐10 and IL‐4 were measured at baseline, 6, and 12 months. Intention‐to‐treat (ITT) analysis was performed using linear mixed models adjusted for baseline biomarker concentrations. Circulating anti‐inflammatory cytokine levels decreased among all groups, with percent change ranging from −3.4% (controls) to −8.2% (HIGH) for IL‐4 and −1.6% (controls) to −7.5% (HIGH) for IL‐10. No significant group differences were found for IL‐4 (ALPHA P = 0.54; BETA P = 0.32) or IL‐10 (ALPHA P = 0.84; BETA P = 0.68). Some evidence for moderation of the effect of exercise by baseline characteristics was found for IL‐10 but not for IL‐4. Results from these two large randomized aerobic exercise intervention trials suggest that aerobic exercise does not alter IL‐10 or IL‐4 in a manner consistent with chronic disease and cancer prevention. The mechanisms whereby regular exercise reduces chronic inflammation remain unclear. We investigated whether regular aerobic exercise alters basal levels of interleukin (IL)‐10 and IL‐4 in two randomized trials of physical activity. Results from these two large randomized aerobic exercise intervention trials suggest that aerobic exercise does not alter IL‐10 or IL‐4 in a manner consistent with chronic disease and cancer prevention.

Obesity considered being a low-grade inflammatory disease. The objective of this study was to examine the association between inflammatory markers (IM) including C-reactive protein (hs-CRP), Interleukin-6 (IL-6), and homocystein (Hcy) and obesity-related factors (e.g. BMI, waist, hip) in adult participants of Tehran lipid and glucose study (TLGS). In this cross-sectional study, 352 individuals (132 men and 220 women), age ≥19 years, were randomly recruited from participants of TLGS population. The serum levels of hs-CRP, IL-6, Hcy were determined using the enzyme linked immunosorbent assay (ELISA) method. Variables were compared by sample t-test. Bivariate linear correlation was estimated using Pearson's correlation coefficient. Linear regression analysis was applied to investigate the association between IMs and anthropometric and biochemical variables. The mean age of participants was 46.1±16.1 years. abdominal obesity was present in 199(56.5%) individuals. levels of hs-CRP and IL-6 increased in the abdominally obese group (1507±3.3 vs. 577.8±4.3 ng/ml P<0.001) (3.6±3.3 vs. 1.9±3.8 pg/ml P< 0.001), and in the same group, the best predictors for hs-CRP, IL-6 and Hcy were waist (WC), waist to height ratio (WHtR) and wrist respectively; hip and WHtR were the best predictors for Hcy and hs-CRP in the normal group. A linear augmentation in hs-CRP and IL-6 levels was observed in association with obesity categorizes. This study provides evidence that abdominally obese individuals had higher levels of IMs. Wrist, waist and WHtR were the best predictors for Hcy, hs-CRP and IL-6 respectively in this group.

BackgroundPatients with Type 1 Diabetes Mellitus (T1DM) are at increased risk for severe COVID-19 due to chronic inflammation, immune dysregulation, and impaired antiviral responses. However, the combined contribution of cytokine imbalance, host genetic variation, and systemic inflammation on COVID-19 severity in this population remains incompletely understood. This study aimed to investigate inflammatory biomarkers, interleukin profiles and immunogenetic factor associated with COVID -19 outcomes in T1DM patients.MethodsA total of 220 individuals were enrolled, including 160 T1DM patients with confirmed COVID-19 and 60 healthy controls. Serum concentrations of IL-6, IL-10, IL-12A, and IL-18 were quantified using ELISA, along with clinical inflammatory markers (CRP, D-dimer, and NLR). Genetic polymorphisms in the IL-10, IL-12A, IL-6, and IL-18 genes were analyzed using PCR-ARMS. Statistical analyses included group comparisons and correlation analysis. In addition, supervised machine-learning (ML) approaches (Decision Tree and Random Forest) were applied within the T1DM COVID-19 cohort to identify biomarkers predictive of disease severity.ResultsPatients exhibited significantly elevated cytokine levels and inflammatory markers compared to controls (all p < 0.001). The IL-10 polymorphism (rs1800872) was significantly associated with increased disease susceptibility, with the G allele conferring a higher risk (p<0.0001, OR = 2.85 CI95% [1.83-4.43]). IL-12 correlated positively with IL-18 (r = 0.41, p < 0.001) and negatively with IL-6 (r = −0.22, p = 0.005). ML analyses identified IL-18, CRP, and IL-6 as the most informative biomarkers of COVID-19 severity, with IL-18 showing the highest feature importance (0.276, 0.202, and 0.175, respectively).ConclusionThis study highlights the critical role of inflammatory biomarkers and host genetic factors in COVID-19 severity among T1DM patients and identifies IL-18 as a robust and clinically relevant biomarker for risk stratification.

Previous research has shown that nutrients and certain food items influence inflammation. However, little is known about the associations between diet, as a whole, and inflammatory markers. In the present study, we examined the ability of a FFQ-derived dietary inflammatory index (DII) to predict inflammation. Data from a Belgian cross-sectional study of 2524 generally healthy subjects (age 35–55 years) were used. The DII is a population-based, literature-derived dietary index that was developed to predict inflammation and inflammation-related chronic diseases. The DII was calculated from FFQ-derived dietary information and tested against inflammatory markers, namely C-reactive protein (CRP), IL-6, homocysteine and fibrinogen. Analyses were performed using multivariable logistic regression, adjusting for energy, age, sex, BMI, smoking status, education level, use of non-steroidal anti-inflammatory drugs, blood pressure, use of oral contraceptives, anti-hypertensive therapy, lipid-lowering drugs and physical activity. Multivariable analyses showed significant positive associations between the DII and the inflammatory markers IL-6 (>1·6 pg/ml) (OR 1·19, 95 % CI 1·04, 1·36) and homocysteine (>15 μmol/l) (OR 1·56, 95 % CI 1·25, 1·94). No significant associations were observed between the DII and the inflammatory markers CRP and fibrinogen. These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation.