Concentrations Of Inflammatory Markers Research Articles

Comparison of early pregnancy serum concentration of neopterin, neopterin/creatinine ratio, C-reactive protein, and chitotriosidase, in pregnant women with birth at term and spontaneous preterm birth.

Inflammatory mechanisms are involved in achieving a normal pregnancy and in the development of certain pregnancy complications. These changes are more intense in pregnant women that suffer of pregnancy complications, such as spontaneous preterm birth (SPB). This study compared the course of inflammatory markers (IM) [neopterin (Neo), neopterin/creatinine ratio (Neo/Cre), C-reactive protein (CRP), and chitotriosidase (Chito)] serum concentration in the early pregnancy of women with birth at term (BT) and preterm birth (PB). IM concentration was measured in 90 sera sampled from 45 pregnancies with BT and 30 sera from 15 pregnancies with PB. Two sera were sampled from each pregnant woman: one in the first trimester and another one in the second trimester. Early pregnancy IM concentration showed a direct correlation with gestational age: Neo (rho=0.262, P=0.004), Neo/Cre (rho=0.372, P<0.001), CRP (rho=0.187, P=0.041), and Chito (rho=0.039, P=0.66). The correlation was present in both categories of patients with BT and PB. Patients with PB before 34 week of pregnancy (wp) and 32 wp showed higher Neo and Neo/Cre concentration than BT patients. A significant association was found between the risk of PB before 34 wp, PB before 32 wp, and Neo concentration (PB <34 wp: odds ratio (OR) =5.13, P=0.035) (PB <32 wp: OR=8.2, P=0.020) and, respectively, Neo/Cre concentration (PB <34 wp: OR=5.29, P=0.015) (PB <32 wp: OR=9.25, P=0.006). No association between CRP or Chito and PB age was found. IM concentration correlates with the gestational age at the time of blood sampling. Increased Neo and Neo/Cre concentration are associated with PB. Further studies are needed to evaluate the usefulness of these markers in clinical practice.

A new potential mode of cardiorenal protection of KLOTHO gene variability in type 1 diabetic adolescents

As the KL-VS haplotype alters secretion and activity of KLOTHO and uric acid (UA) is associated with endothelial dysfunction and inflammation, their mutual links may contribute to microalbuminuria (MA) in patients with type 1 diabetes (T1D). Therefore, we hypothesize that KL-VS polymorphism could be associated with the prevalence of MA in T1D patients, and KL-VS polymorphism could modify physiological functions and pathogenic potential of UA. We have examined 350 patients with T1D. The analysis concerned KL-VS polymorphism along with the concentrations of serum inflammatory markers, indicators of renal function, blood pressure, and lipid profile. The incidence of KL-VS genotype was lower in a group with MA in comparison to patients without this condition. Moreover, KL-VS carriers had improved indicators of renal function, lower concentrations of pro-inflammatory cytokines, and higher levels of anti-inflammatory markers. Simultaneously, among KL-VS carriers serum UA was negatively correlated with HbA1c, albumin excretion rate, ACR, CRP, TNF-α, total cholesterol, LDL-C and triglycerides, and positively correlated with HDL-C. Moreover, among wild-type KLOTHO carriers serum, UA was in positive correlation with creatinine, blood pressure, IL-12 and MCP-1, and in negative correlation with IL-10 and eGFR. Findings of our study suggest that the functional KL-VS polymorphism is independently associated with MA and the KL-VS genotype protects from the development of MA, and KL-VS polymorphism may modify physiological functions and pathogenic potential of UA by altering the levels of HbA1c, inflammatory biomarkers, indicators of renal function, blood pressure, and lipid profile.Key messages• We analyzed the KL-VS polymorphism and the UA serum level in patients with T1D.• The KL-VS polymorphism is independently associated with microalbuminuria.• The KL-VS alleles protect from the development of microalbuminuria.• KL-VS polymorphism may modify physiological functions and pathogenic potential of uric acid.

Protein and gene markers of metabolic dysfunction and inflammation together associate with functional connectivity in reward and motor circuits in depression

Bidirectional relationships between inflammation and metabolic dysfunction may contribute to the pathophysiology of psychiatric illnesses like depression. Metabolic disturbances drive inflammation, which in turn exacerbate metabolic outcomes including insulin resistance. Both inflammatory (e.g. endotoxin, vaccination) and metabolic challenges (e.g. glucose ingestion) have been shown to affect activity and functional connectivity (FC) in brain regions that subserve reward and motor processing. We previously reported relationships between elevated concentrations of endogenous inflammatory markers including C-reactive protein (CRP) and low corticostriatal FC, which correlated with symptoms of anhedonia and motor slowing in major depression (MD). Herein, we examined whether similar relationships were observed between plasma markers related to glucose metabolism (non-fasting concentrations of glucose, insulin, leptin, adiponectin and resistin) in 42 medically-stable, unmedicated MD outpatients who underwent fMRI. A targeted, hypothesis-driven approach was used to assess FC between seeds in subdivisions of the ventral and dorsal striatum and a region in ventromedial prefrontal cortex (VS-vmPFC), which was previously found to correlate with both inflammation and symptoms of anhedonia and motor slowing. Associations between FC and gene expression signatures were also explored. A composite score of all 5 glucose-related markers (with increasing values reflecting higher concentrations) was negatively correlated with both ventral striatum (VS)-vmPFC (r = −0.33, p < 0.05) and dorsal caudal putamen (dcP)-vmPFC (r = −0.51, p < 0.01) FC, and remained significant after adjusting for covariates including body mass index (p < 0.05). Moreover, an interaction between the glucose-related composite score and CRP was observed for these relationships (F[2,33] = 4.3, p < 0.05) whereby significant correlations between the glucose-related metabolic markers and FC was found only in patients with high plasma CRP (>3 mg/L; r = −0.61 to −0.81, p < 0.05). Insulin and resistin were the individual markers most predictive of VS-vmPFC and dcP-mPFC FC, respectively, and insulin, resistin and CRP clustered together and in association with both LV-vmPFC and dcP-vmPFC in principal component analyses. Exploratory whole blood gene expression analyses also confirmed that gene probes negatively associated with FC were enriched for both inflammatory and metabolic pathways (FDR p < 0.05). These results provide preliminary evidence that inflammation and metabolic dysfunction contribute jointly to deficits in reward and motor circuits in MD. Future studies using fasting samples and longitudinal and interventional approaches are required to further elucidate the respective contributions of inflammation and metabolic dysfunction to circuits and symptoms relevant to motivation and motor activity, which may have treatment implications for patients with psychiatric illnesses like depression.

Effects of Vitamin D Status on Inflammatory Markers in Obese Subjects: A Systematic Review

Background: Recent studies have demonstrated the role of micronutrients in the manifestation of comorbidities associated with obesity. Vitamin D deficiency, in particular, appears to be associated with increased levels of inflammatory markers, which may lead to chronic low-grade inflammation, elevating the risk of chronic diseases such as diabetes, metabolic syndrome, and cardiovascular disease. The objective of this study was to perform a systematic review of observational studies conducted to investigate the effect of vitamin D deficiency on inflammatory markers in obese subjects. Methodology: This systematic review was conducted in accordance with the “STROBE” and PRISMA recommendations. Observational studies that evaluated the effect of vitamin D status on inflammatory markers in obese subjects were selected and reviewed. Searches were conducted in the PubMed, SciVerse Scopus, and Web of Science databases from February 21 to 22, 2018. Results: After the selection and removal of duplicate articles, 10 eligible articles were identified. Results from eight observational studies showed an association between vitamin D deficiency or insufficiency in the body and increased concentrations of inflammatory markers in obese individuals. On the other hand, two of the studies did not demonstrate any correlation. With regard to the inflammatory markers evaluated, eight studies showed high concentrations of ultra-sensitive C-reactive protein, five studies found an increase in interleukin-6 concentrations, and two studies noted increased levels of tumor necrosis factor. Conclusion: The data presented in this systematic review provide evidence of the association between vitamin D deficiency and increased inflammation in obesity.

Markers of inflammation and insulin resistance in dogs before and after weight loss versus lean healthy dogs

ABSTRACT: Chronic low-grade inflammation in obesity is characterized by an increased production of pro-inflammatory cytokines that contribute to insulin resistance. For this study body composition, markers of inflammation and of insulin resistance in dogs before and after weight loss were compared to those of lean dogs. Eleven client-owned obese adult dogs underwent a weight loss program with commercial dry food for weight loss and reached an ideal body condition score (BCS) six months after the beginning of the weight loss program. A Control Group of nine dogs with ideal BCS were selected for the comparison. Shapiro-Wilk test was used to test for normality, Mann Whitney were used for non-normally distributes data, and Student t-test was used for normally distributed parameters. In the Obese Group body fat decreased from 41.6% (30.7-58.6) to 29.1% (18.6-46.3) (P&lt;0.01) and dogs maintained lean body mass throughout the weight loss program (P&gt;0.05). Obese dogs presented higher concentration of fructosamine, triglycerides, insulin, IGF-1 and leptin than the Control Group before weight reduction (P&lt;0.05). Serum concentrations of triglycerides, IL-2, IL-6, TNF-α, insulin, leptin and IGF-1 decreased after weight loss (P&lt;0.01), and these concentrations were similar to the Control Group (P&gt;0.05), except for leptin (P&lt;0.001). No alteration on peptide YY was found. Leptin (r=0.60, P=0.01), fructosamine (r=0.44, P=0.02) and triglycerides (r=0.40, P=0.04) concentrations correlated with the reduction of body fat. Weight loss reduced the concentrations of inflammatory and insulin resistance markers and most parameters became similar to dogs that have always been lean, reinforcing the importance of weight loss in small animal practice.

Obesogenic diet-associated C-reactive protein predicts reduced central dopamine and corticostriatal functional connectivity in female rhesus monkeys

Alterations in dopamine (DA) signaling and reductions in functional connectivity (FC; a measure of temporal correlations of activity between different brain regions) within dopaminergic reward pathways are implicated in the etiology of psychopathology and have been associated with increased concentrations of inflammatory markers, including C-reactive protein. Peripheral and central inflammatory cytokines that have been shown to disrupt DA signaling and corticostriatal FC are associated with C-reactive protein, an acute phase reactant that is used translationally as a marker of systemic inflammation. One factor that can significantly increase systemic inflammation to produce neuroadaptations in reward pathways is a diet that results in fat mass accumulation (e.g. obesogenic diet). The current study in female rhesus monkeys maintained in a standard laboratory chow (n = 18) or on obesogenic diet (n = 16) for 12-months tested the hypothesis that an obesogenic diet would alter central DA and homovanillic acid (HVA) concentrations, and be associated with increased CRP concentrations and decreased FC between corticostriatal regions at 12-months following dietary intervention. We specifically assessed FC between the nucleus accumbens (NAcc) and two sub-regions of the prefrontal cortex (PFC) previously associated with CRP concentrations, the ventromedial PFC (vmPFC) and the orbitofrontal cortex (OFC), which are also involved in emotional and motivational salience assessment, and in goal-directed behavior, impulse control and the salience/value of food, respectively. Results showed that CSF DA concentrations were decreased (p = 0.002), HVA:DA ratios were increased (p = 0.016), and body mass index was increased (p = 0.047) over the 12-months of consuming an obesogenic diet. At 12-months, females maintained in the obesogenic diet exhibited higher CRP concentrations than females consuming chow-only (p = 0.008). Linear regression analyses revealed significant CRP by dietary condition interactions on DA concentrations (β = −5.10; p = 0.017) and HVA:DA ratios (β = 5.14; p = 0.029). Higher CRP concentrations were associated with lower CSF DA concentrations (r = −0.69; p = 0.004) and greater HVA:DA ratios only in females maintained in the obesogenic dietary condition (r = 0.58; p = 0.024). Resting-state magnetic resonance neuroimaging (rs-fMRI) in a subset of females from each diet condition (n = 8) at 12-months showed that higher CRP concentrations were associated decreased FC between the NAcc and subregions of the prefrontal cortex (PFC; p’s < 0.05). Decreased FC between the NAcc and PFC subregions were also associated with lower concentrations of DA and greater HVA:DA ratios (p’s < 0.05). Overall, these data suggest that increased inflammatory signaling driving heightened CRP levels may mediate the adverse consequences of obesogenic diets on DA neurochemistry and corticostriatal connectivity.

Relationship among the leptin-to-adiponectin ratio, systemic inflammation, and anisocytosis in well-controlled type 2 diabetic patients with atherosclerotic cardiovascular disease.

Previous studies have shown that red blood cell distribution width (RDW) is an independent predictor of poor prognosis in type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). The mechanisms underlying increased anisocytosis in patients with T2D and confirmed ASCVD remain poorly understood. We sought to evaluate the relationship among the leptin-to-adiponectin ratio, systemic low -grade inflammation, and RDW in optimally treated patients with T2D and established ASCVD. A total of 68 patients, aged 47 to 85 years (mean [SD], 65.3 [6.8] years) and including 21 women (30.9%), were enrolled and grouped according to median RDW into those with RDW <13.5% (n = 33) and those with RDW ≥13.5% (n = 35). Patients with RDW ≥13.5% had a significantly higher median (interquartile range [IQR]) serum leptin-to-adiponectin ratio (1.7 [0.49-2.3] ng/μg vs 0.66 [0.31-1.25] ng/μg; P = 0.04) and median (IQR) tumor necrosis factor α levels (1.58 [1.42-1.97] pg/ml vs 1.39 [1.18-1.57] pg/ml; P = 0.02). There were no significant differences in the concentrations of other inflammatory markers. The leptin-to-adiponectin ratio (r = 0.25; P = 0.04) and levels of tumor necrosis factor α (r = 0.32; P = 0.01) and soluble intercellular adhesion molecule 1 (r = 0.31; P = 0.01) were positively correlated with RDW, which was confirmed by univariate linear regression analysis. A multivariable regression model, which included demographic, clinical, and laboratory data, showed that white blood cell count (β = 0.25; 95% CI, 0.05-0.45; P = 0.01), soluble intercellular adhesion molecule 1 levels (β = 0.21; 95% CI, 0.02-0.41; P = 0.03), and mean corpuscular hemoglobin concentration (MCHC), (β = -0.48; 95% CI, 0.67 to -0.28; P < 0.001) were independent predictors of RDW in our patients. In well-controlled patients with T2D and ASCVD, the RDW values are associated with leptin-to-adiponectin imbalance and selected inflammatory markers.

Effect of anti-inflammatory treatment on systemic inflammation, immune function, and endometrial health in postpartum dairy cows

Systemic inflammation (SI) is increasingly studied in several species because it may be central in many metabolic disturbances and be a risk factor for clinical disease. This proof-of-concept study evaluated the effects of the anti-inflammatory drug meloxicam on markers of SI and energy metabolism, polymorphonuclear neutrophil (PMN) function, and endometritis in clinically healthy postpartum dairy cows. Cows received meloxicam (0.5 mg/kg of body weight; n = 20) once daily for 4 days (10–13 days postpartum) or were untreated (n = 22). Blood samples were collected −7, 1, 3, 5, 7, 10, 11, 12, 13, 14, 18, 21, 28, and 35 days relative to calving to measure serum concentrations of metabolic and inflammatory markers. Function of peripheral blood PMN were evaluated at 5, 10, 14, and 21, and proportion of PMN in endometrial cytology were performed at 5, 10, 14, 21, 28 and 35 days postpartum. Meloxicam decreased serum haptoglobin from the second until the last day of treatment, and improved indicators of energy metabolism (lesser β-hydroxybutyrate and greater insulin-like growth factor-1 during treatment, and greater glucose at the end of treatment than control cows). This improved PMN function at 14 days postpartum, but the endometrial inflammatory status was not affected.

Inflammation, Hippocampal Volume, and Therapeutic Outcome following Electroconvulsive Therapy in Depressive Patients: A Pilot Study

Introduction: Electroconvulsive therapy (ECT) influences the concentration of peripheral inflammatory markers, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In which way this immune effect contributes to the impact of ECT on the central nervous system in depression remains unknown. Objective: The aim of this study was to examine whether the hippocampal volumetric increase in depressed patients treated with ECT is related to changes in peripheral IL-6 and TNF-α levels. Methods: IL-6 and TNF-α plasma levels were measured in 62 patients 1 week before and after an acute course of ECT. Hippocampal volumes were analyzed in a magnetic resonance imaging (MRI) subsample of 13 patients at the same time points. Results: A significant decrease in IL-6 levels was observed in the total sample and a significant increase in hippocampal volume in the MRI subsample. The reduction of peripheral IL-6 correlated with an increase in total hippocampal volume. A more limited decrease of TNF-α correlated with a more limited increase of both the total and left hippocampus volumes. Conclusion: This pilot study is the first to highlight the link between peripheral immune changes and hippocampal volume increase following ECT. Further research is required to conclude whether ECT indeed exerts its central effect on the brain via changes of peripheral inflammatory markers.

Massage Therapy Modulates Inflammatory Mediators Following Sprint Exercise in Healthy Male Athletes

Massage therapy is a common postexercise muscle recovery modality; however, its mechanisms of efficacy are uncertain. We evaluated the effects of massage on systemic inflammatory responses to exercise and postexercise muscle performance and soreness. In this crossover study, nine healthy male athletes completed a high-intensity intermittent sprint protocol, followed by massage therapy or control condition. Inflammatory markers were assessed pre-exercise; postexercise; and at 1, 2, and 24 h postexercise. Muscle performance was measured by squat and drop jump, and muscle soreness on a Likert scale. Significant time effects were observed for monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), drop jump performance, squat jump performance, and soreness. No significant effects for condition were observed. However, compared with control, inflammatory marker concentrations (IL-8, TNFα, and MCP-1) returned to baseline levels earlier following the massage therapy condition (p < 0.05 for all). IL-6 returned to baseline levels earlier following the control versus massage therapy condition (p < 0.05). No differences were observed for performance or soreness variables. MCP-1 area under the curve (AUC) was negatively associated with squat and drop jump performance, while IL-10 AUC was positively associated with drop jump performance (p < 0.05 for all). In conclusion, massage therapy promotes resolution of systemic inflammatory signaling following exercise but does not appear to improve performance or soreness measurements.

Analyses of interleukin-6, presepsin and pentraxin-3 in the diagnosis and severity of late-onset preeclampsia

Introduction The etiology/pathophysiology of preeclampsia remains an enigma. Maternal inflammation (humoral and cellular) is a key factor in the etiology of late-onset preeclampsia (L-PrE). Presepsin is split out from the phagocytes membranes after phagocytosis. It is known as a novel inflammation marker. To our knowledge, this is the first study in literature in English to investigate maternal blood concentrations of presepsin in preeclampsia and healthy pregnant women. Methods We examined maternal plasma interleukin-6, presepsin and pentraxin-3 concentrations in pregnant women with (n = 44) and without L-PrE (n = 44). These three inflammatory markers concentrations measured using enzyme-linked immunosorbent assays were compared. Results The mean maternal age and gestational age at sampling are similar in the both groups (p ≥ .05). Interleukin-6, presepsin and pentraxin-3 concentrations differed between the groups (p < .05). There was no difference between the three inflammatory markers concentrations in patients with mild (22 patients) and severe (22 patients) preeclampsia in L-PrE (p ≥ .05). A significant discriminative role of interleukin-6, presepsin and pentraxin-3 for presence of L-PrE, with cutoff values of 39.74 pg/mL, 309.88 mg/L and 34.96 ng/mL, respectively, were reported in a ROC curve analysis. When the patients with and without small for gestational age infants (12 patients and 76 patients, respectively) were compared, it was determined that there was no differences between the interleukin-6, but there were differences between the presepsin and pentraxin-3 concentrations (p = .016, p = .008, respectively). Conclusion Lower concentrations of interleukin-6/presepsin and higher concentrations of pentraxin-3 were associated with the development of preeclampsia. Further investigations of inflammatory/immunity markers in pregnancy are required and may ultimately lead to novel therapeutic approaches to treat complications of pregnancy.

Oral supplementation with omega-3 fatty acids and inflammation markers in patients with chronic kidney disease in hemodialysis

Chronic kidney disease (CKD) is an increasingly common public health problem that increases the risk of death because of cardiovascular complications by 2-3 times compared with the general population. This research concerns a prospective, randomized, double-blind study in patients with CKD undergoing hemodialysis. The participants were assigned to 1 of 2 groups: the study group (group A; 46 patients) received 4 capsules (2.4 g) of omega-3 fatty acids daily during the 12-week intervention, while patients in the control group (group B; 47 patients) received 4 capsules of paraffin oil. The patients' general characteristics, nutritional indicators, renal disease markers and inflammatory markers (C-reactive protein, interleukin (IL)-6, IL-10, and tumour necrosis factor alpha (TNF-α)) were evaluated. No differences were found between the general characteristics of the patients (P < 0.05), and no differences were shown in the nutritional indicators and markers of kidney disease (P < 0.05). Patients in group A showed significant decreases in levels of C-reactive protein, IL-6, TNF-α, and the IL-10/IL-6 ratio after 12 weeks of supplementation (P < 0.05). Patients in group B did not show any significant changes in concentrations of inflammatory markers during the intervention (P < 0.05). In conclusion, oral supplementation with omega-3 fatty acids produces a significant decrease in the concentrations of inflammation markers in patients with chronic kidney disease on hemodialysis. Novelty Oral supplementation with omega-3 fatty acids produced significant decreases in the concentrations of inflammation markers. This supplementation could be given to patients with uremic syndrome and coronary heart disease to reduce cardiovascular risk.

Serum level of sVAP-1 in relation to the severity of inflammation, predictive marker of prognosis in patients scheduled for colorectal surgery

Background: VAP-1, like other adhesion molecules, can exist as soluble circulating form (sVAP-1). Elevated serum sVAP-1 levels were observed in both type 1 and type 2 diabetic patients, in subjects with primary biliary cirrhosis and alcoholic liver cirrhosis, while patients with rheumatoid arthritis or inflammatory bowel disease did not exhibit significant alterations in sVAP-1 level when compared to healthy individuals. Only scarce and controversial information is available on the serum sVAP-1 levels in cases of malignant neoplasms. The purpose of our study was to assess the relationship between the level of soluble vascular adhesion protein 1 and the concentration of inflammatory markers, as well as to assess the predictive value of sVAP-1 in patients with colorectal cancer scheduled for surgery. Methods: Kaplan-Meier analysis and log-rank test were performed to assess the correlation between sVAP-1 levels and the clinical outcomes on disease-free survival (DFS). Results: Compared to healthy individuals, patients suffering from colorectal cancer, expressed a significantly lower levels of sVAP-1 (p &lt; 0.000002) and significantly higher concentrations of CEA (p = 0.003), IL-6 (p = 0.0001), CRP (p = 0.0001), AAG (p = 0.0001), and haptoglobin (p = 0.0001) in the serum. In the studied group of patients, a significant negative correlation between the serum levels of sVAP-1 vs. CRP (r = – 0.195; p = 0.031), sVAP-1 vs. AAG (r = – 0.234; p = 0.009), sVAP-1 vs. HAP (r = – 0.226; p = 0.012) were found. 3-year DFS of the patients with pretreatment levels of CEA ≥ 5 μg/L was significantly lower than the patients with pretreatment levels of CEA &lt; 5 μg/L (47.4% vs. 82.9%, p = 0.00005). 3-year DFS of patients with pretreatment concentrations of sVAP-1≤ 185 μg/L was significantly lower than the patients with pretreatment concentrations of sVAP-1 &gt; 185 μg/L (59.4% vs. 77.4%, p = 0.0378). Conclusions: In patients scheduled for colorectal cancer surgery, serum concentrations of sVAP-1 are related to the tumour stage and the severity of acute phase reaction. Increased CEA concentrations or decreased sVAP-1 levels before surgery is associated with shorter time to disease progression following resection of colorectal cancer.

Ultra-endurance triathlon performance and markers of whole-body and gut-specific inflammation.

To examine the influence of the Ultraman Florida triathlon (3days of non-continuous racing; stage 1: 10km swim and 144.8km cycle; stage 2: 275.4km cycle; stage 3: 84.4km run) on circulating plasma concentrations of whole-body (C-reactive protein (CRP), interleukin (IL)-6 (IL-6), and IL-10 and surrogate gut-specific inflammatory markers (IL-17 and IL-23), and determine whether these variables are associated with performance. Eighteen triathletes (N = 18; 15 men, 3 women; age: 37 ± 8 yrs) were evaluated at baseline and post-race for circulating concentrations of CRP, IL-6, IL-10, IL-17, and IL-23. Blood samples were drawn two days prior to stage 1 (1600h) and one day after stage 3 (1200h). Plasma CRP significantly increased from baseline (1985.8 ± 5962.3ng/mL) to post-race (27,013.9 ± 12,888.8ng/mL, p < 0.001, 13-fold increase). Both plasma IL-6 and IL-10 did not significantly change from baseline to post-race. Baseline and post-race concentrations of IL-17 and IL-23 were below detectable limits. Pearson's correlation between mean finish time and post-race IL-10 revealed a significant positive correlation (r = 0.54, p < 0.05). Our results suggest that cytokines such as IL-6 and IL-10 involved in the inflammatory response return to near-baseline concentrations rapidly even after ultra-endurance events of extreme duration. The absence of IL-17 and IL-23 may suggest positive gut adaptations from ultra-endurance training. A significant positive correlation between post-race IL-10 concentrations and mean finish time may indicate that a relationship between anti-inflammatory responses and performance exists.

Systemic inflammatory response to the Radial Pressure Wave Therapy (RPWT) in collagenase-induced Achilles tendinopathy treated with Adipose Derived Stem Cells or Platelet Rich Plasma

Novel tendinopathy treatment protocols should be assessed for safety. The goal of this work was to compare differences in selected systemic inflammatory marker concentrations after two treatment protocols for collagenase induced Achilles tendinopathy in sheep. 14 sheep (aged 5 and 6 years, Polish Mountain Sheep breed, weight 60-70kg) were injected with bacterial collagenase type 1A-S (Clostridium histolyticum, C-5894, Sigma Aldrich, Poznań, Poland) bilaterally to Achilles tendons. Subsequently, the animals were injected with Platelet Rich Plasma (7 sheep) or Adipose Derived Stem Cells (7 sheep) to induced tendinopathy foci. Left limbs of all sheep were additionally treated with Radial Pressure Wave Therapy (RPWT) focused above the tendinopathy origins. Treatment progress was controlled by ultrasound scans, and tendon samples were taken on the 126th day of the experiment. Serum Amyloid A (SAA) concentration showed mild elevation before the experiment (2 sheep from group I, 4 sheep from group II) and two days after the intratendinous growth factors injection ( 4 sheep from group I, 3 sheep from group II) combined with RPWT (mean 22,63 mg/L and 53, 6 mg/L respectively). Haptoglobine (Hp) concentration increased from 0 to 0,01 g/L in 2 animals from group I two days after injection. These values declined to 0 during the course of the treatment. Fibrinogen (Fb) concentrations were within reference levels throughout the research, although mild elevation was observed before the treatment course in 6 sheep from group I and 1 sheep from group II. In conclusion, addition of RPWT to growth factors injections in the treatment of yatrogenic Achilles tendinopathy in sheep did not induce systemic inflammatory response.

Effects of rumen-protected choline on the inflammatory and metabolic status and health of dairy cows during the transition period

The objectives of this study were to evaluate the effects of rumen-protected choline (RPC) supplementation from 21 d pre- to 21 d postpartum on markers of metabolic status and inflammatory response, concentrations of liposoluble vitamins, and plasma total Ca in parous Holstein cows. The hypotheses were that supplementing RPC during the transition period would reduce hepatic triacylglycerol accumulation postpartum and attenuate markers of inflammatory response following parturition, and collectively, such responses were expected to benefit health of dairy cows. Parous cows at 241 d of gestation were blocked by parity group and 305-d milk yield, and within block, they were assigned randomly to receive either 0 g/d [no choline in transition (NT), n = 55] or 12.9 g/d choline ion [choline in transition (CT), n = 58] from 21 d pre- to 21 postpartum. The RPC product was individually top-dressed onto the total mixed ration once daily. Prepartum, treatments were supplemented (mean ± standard deviation) for the last 18.8 ± 5.7 and 19.2 ± 5.0 d of gestation in NT and CT, respectively. Supplementing RPC prepartum did not affect concentrations of plasma metabolites and inflammatory markers during the last 3 wk of gestation. Postpartum, cows fed RPC had greater hepatic concentration of hepatic triacylglycerol (NT = 3.4 vs. CT = 4.4%) and tended to have increased concentration of β-hydroxybutyrate (NT = 0.48 vs. CT = 0.53 mM) in plasma. In spite of the increased hepatic triacylglycerol in cows fed RPC, treatment did not affect the concentrations of the inflammatory marker tumor necrosis factor-α or of the positive acute phase proteins, haptoglobin and fibrinogen. Supplementing choline tended to increase the concentration of plasma triacylglycerol by 0.69 mg/dL in the first 21 d postpartum and reduced the incidence of subclinical hypocalcemia by 20.9 percentage units compared with NT. Supplementing transition cows with RPC did not affect the concentrations of liposoluble vitamins in the first 7 d postpartum or the incidence of individual diseases or morbidity in early lactation. The inability of supplemental choline to reduce hepatic triacylglycerol might have been a consequence of the increased productive performance without additional dry matter intake.

Diet Based on Food from the Colombian Andean Region Decreases C-reactive Protein, IL6, and Leptin in Women with Obesity

People with obesity develop low-grade chronic inflammation, which is characterized by a high serum concentration of inflammatory markers (CRP, IL-6, TNF-α, and leptin), which predisposes the development of chronic diseases. These markers can be modulated by a diet; therefore, a research project was developed to determine the effect of a diet based on foods available in the Colombian Andean Region, containing anti-inflammatory properties in obese women. A controlled study was conducted with 30 women. For eight weeks the experimental group received a diet based on food rich in fiber, polyunsaturated fatty acids, vitamins and polyphenols. The experimental group reduced the serum concentrations of CRP (p = 0.005), IL-6 (p = 0.013) and leptin (p = 0.004), in comparison with the control group. Therefore, the findings suggest that a diet based on foods available in the Colombian Andean Region with anti-inflammatory nutrients reduces CRP, IL-6 and leptin in obese women.

Associations of inflammatory markers and vascular cell adhesion molecule-1 with endothelial dysfunction in collagen-induced arthritis

We determined the role of high-grade inflammation on endothelial function and its association with biomarkers of endothelial dysfunction in collagen-induced arthritis. Sprague-Dawley rats were divided into a control (n = 12) or collagen-induced arthritis (CIA; n = 21) group. To induce arthritis, Bovine-type-II collagen emulsified in incomplete Freund's adjuvant was injected at the base of the tail. Nine-weeks after the primary immunisation, vascular reactivity in mesenteric and saphenous arteries was assessed using a wire-myograph. Serum concentrations of inflammatory markers (tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), interleukin 1β (IL-1β), C-reactive protein (CRP)) and biomarkers of endothelial dysfunction (vascular cell adhesion molecule-1 (VCAM-1) and asymmetric dimethylarginine (ADMA)) were measured by ELISA. Acetylcholine-induced relaxation in mesenteric and saphenous arteries was impaired in CIA compared to controls (P < 0.05). Responses to sodium nitroprusside were similar between controls and CIA in mesenteric arteries and marginally impaired in saphenous arteries of CIA rats. Compared to controls, TNF-α, IL-6, IL-1β, CRP (all P < 0.00001) and VCAM-1 (P = 0.02) were elevated in CIA. TNF-α (std β(SE) = 0.39(0.16); P = 0.03), IL-6 (std β(SE) = 0.37(0.17); P = 0.03), IL-1β (std β(SE) = 0.41(0.16); P = 0.02) and CRP (std β(SE) = 0.36(0.17); P = 0.04) were associated with VCAM-1. Associations between inflammatory markers and the maximal relaxation (Emax) to acetylcholine in mesenteric arteries were no longer significant after adjusting for VCAM-1 (except for IL-1β). VCAM-1 was inversely associated with the Emax to acetylcholine in mesenteric (std β(SE) = -0.49(0.16); P = 0.01) but not in saphenous arteries (std β(SE) = -0.06(0.18); P = 0.76). In conclusion, exposure to high-grade inflammation impairs endothelial-dependent relaxation. The inflammation-induced increase in VCAM-1 concentrations may contribute to the impaired endothelium-dependent relaxation in mesenteric arteries of CIA rats.

Intraoperative Flurbiprofen Treatment Alters Immune Checkpoint Expression in Patients Undergoing Elective Thoracoscopic Resection of Lung Cancer

Objectives: This study aimed to determine the effect of intraoperative administration of flurbiprofen on postoperative levels of programmed death 1 (PD-1) in patients undergoing thoracoscopic surgery. Materials and Methods: In this prospective double-blind trial, patients were randomized to receive intralipid (control group, n = 34, 0.1 mL/kg, i.v.) or flurbiprofen axetil (flurbiprofen group, n = 34, 50 mg, i.v.) before induction of anesthesia. PD-1 levels on T cell subsets, inflammation, and immune markers in peripheral blood were examined before the induction of anesthesia (T₀) and 24 h (T₁), 72 h (T₂), and 1 week (T₃) after surgery. A linear mixed model was used to determine whether the changes from baseline values (T₀) between groups were significantly different. Results: The increases in the percentage of PD-1⁽⁺⁾CD8⁽⁺⁾ T cells observed at T₁ and T₂ in the control group were higher than those in the flurbiprofen group (T₁: 12.91 ± 1.65 vs. 7.86 ± 5.71%, p = 0.031; T₂: 11.54 ± 1.54 vs. 8.75 ± 1.73%, p = 0.004), whereas no differences were observed in the changes in the percentage of PD-1⁽⁺⁾CD4⁽⁺⁾ T cells at T₁ and T₂ between the groups. Moreover, extensive changes in the percentage of lymphocyte subsets and inflammatory marker concentrations were observed at T₁ and T₂ after surgery and flurbiprofen attenuated most of these changes. Conclusions: Perioperative administration of flurbiprofen attenuated the postoperative increase in PD-1 levels on CD8⁽⁺⁾ T cells up to 72 h after surgery, but not after this duration. The clinical relevance of changes in PD-1 levels to long-term surgical outcome remains unknown.

Abstract P2064: Changes in Inflammatory Markers Monitored Across Time After Bariatric Surgery in Severely Obese Patients

Adipose tissue is a higly active endocrine tissue and produce adipokines, peptides produced by adipose tissue and exerting autocrine, paracrine and endocrine function. Objective: to analyze changes (Δ) in serum levels of several adipokines and inflammatory markers in morbidly obese patients (MO) after bariatric surgery (BS) at several follow-up time points. Methods: Fifty-two MO (81% women, 40% hypertensives, age 43.9±8.9 yr, BMI 42.2±5.4 Kg/m 2 , waist circumference 131.6±12.1 cm) were evaluated prospectively before and 1,3,6 and 12 months (m) after BS, with assessment of anthropometric data and serum concentrations of several adipokines and inflammatory markers. BS technique: laparoscopic gastric by-pass (28 of 52) and sleeve gastrectomy (24 of 52). Results: at 12m body weight (-35.7±10.2 Kg) and waist circumference (-27.2±9.4 cm) decreased (p&lt;0.001). Two inflammatory markers, leptin and hsCRP, decreased at 1,3,6 and 12m (p&lt;0,005 for all). Adiponectin and angiopoetin-2 increased from month 3 on. (Table). These Δ were statistically significant when examined by an ANOVA with repeated measures, excepte for adiponectin (p=0.065). After adjusting for age, sex, and BS technique, the BS technique was statistically significant only for ΔhsCRP (p=0.035). Pearson correlations were explored. There were no statistically significant correlation between Δ body weight or Δ waist circumference with changes of any of these markers at any follow-up time point. Conclusions: there is a decrease in inflammatory markers 1 m after BS in MO patients with progressive decrease throughout 12 m. These changes are independent of the BS technique and of Δ in body weight and waist circumference.