Microinflammation In Patients Research Articles

Microinflammation in Patients on Hemodialysis: A Practical Approach

Microinflammation in Patients on Hemodialysis: A Practical Approach

Relationship between Compound α-Ketoacid and Microinflammation in Patients with Chronic Kidney Disease.

Chronic kidney disease (CKD) refers to the presence of structural or functional abnormalities in the kidneys that affect health, lasting for more than 3 months. CKD is not only the direct cause of global incidence rate and mortality, but also an important risk factor for cardiovascular disease. Persistent microinflammatory state has been recognized as an important component of CKD, which can lead to renal fibrosis and loss of renal function, and plays a crucial role in the pathophysiology and progression of the disease. Simultaneously, compound α-Ketoacid can bind nitrogen-containing metabolites in the blood and accelerate their excretion from the body, thereby reducing the level of metabolic waste, alleviating gastrointestinal reactions in patients, and reducing the inflammatory response and oxidative stress state of the body. Compound α-Ketoacid contains amino acids required by CKD patients. In this review, we explore the relationship between compound α-Ketoacid and microinflammation in patients with CKD. The review indicated that compound α-Ketoacid can improve the microinflammatory state in CKD patients by improving the nutritional status of CKD patients, improving patient's acid-base balance disorder, regulating oxidative stress, improving gut microbiota, and regulating abnormal lipid metabolism.

Yokukansan Suppresses Gastric Hypersensitivity and Eosinophil-associated Microinflammation in Rats With Functional Dyspepsia.

Background/AimsHerbal medicine is an important complementary therapy for functional dyspepsia (FD). However, its effect against gastric hypersensitivity in patients with FD has rarely been evaluated. Yokukansan (YKS), a traditional Japanese herbal medicine, is effective against neuropathic and inflammatory pain. This study aims to use a maternal separation (MS) stress-induced FD model to investigate the effects of YKS against gastric hypersensitivity, gastric motility, and duodenal micro-inflammation.MethodsThe MS stress model was established by separating newborn Sprague-Dawley rats from their mothers for 2 hours a day from postnatal days 1 to 10. At the age of 7-8 weeks, the rats were treated with YKS at a dose of 5 mL/kg (1 g/kg) for 7 consecutive days. After YKS treatment, electromyographic activity in the acromiotrapezius muscle by gastric distention and the gastric-emptying rate were assessed. Immunohistochemical analysis of eosinophils in the duodenum and phosphorylated extracellular signal-regulated kinase (p-ERK) 1/2 in the spinal cord was performed.ResultsYKS treatment suppressed MS stress-induced gastric hypersensitivity and decreased the elevated levels of p-ERK1/2 in the spinal cord. In the gastroduodenal tract, YKS inhibited eosinophil-associated micro-inflammation but did not improve gastric dysmotility.ConclusionsYKS treatment improved gastric hypersensitivity by alleviating eosinophil-associated micro-inflammation in the gastroduodenal tract. This treatment may be considered an effective therapeutic option for epigastric pain and micro-inflammation in patients with FD.

Duodenal cholinergic tuft cell number is increased in functional dyspepsia

Low-grade duodenal inflammation has recently been identified in patients with functional dyspepsia (FD). Chemosensory tuft cells were reported to be associated with gastrointestinal diseases. We therefore assessed duodenal tuft cell density and microinflammation in patients with FD to determine whether these measures could serve as useful biomarkers, and also correlated tuft cell density and microinflammation in FD patients. Duodenal biopsy specimens were obtained from patients with FD and from controls. Tuft cells, eosinophils, and mast cells were immunochemically stained with specific antibodies. Tuft cells were identified by immunostaining for doublecortin-like kinase 1 (DCLK1); cholinergic tuft cells were assessed by double staining for choline acetyltransferase (ChAT) and DCLK1. Immune-type tuft cells were assessed by IL-25 mRNA expression using real-time PCR. The density of intramucosal eosinophils and mast cells was significantly higher in the duodenum of FD patients than in controls. The density of tuft cells was significantly higher in the duodenum of FD patients compared with controls, and significantly correlated with eosinophil density in the duodenum of FD patients and controls. Moreover, a fraction of ChAT-positive cells was DCLK1 positive; all duodenal DCLK1+ tuft cells were ChAT-immunoreactive in FD and in control subjects. Cholinergic tuft cell density was higher in the duodenum of patients with FD and significantly correlated with eosinophil density. Further studies are needed to investigate the pathophysiological significance of tuft cells in FD and may provide valuable clues to the pathophysiology of FD.

Bruxism Influence on Volume and Interleukin-1β Concentration of Gingival Crevicular Fluid: A Preliminary Study

Bruxism is occlusal behaviour that often leads to stomatognathic system overload. Inflammatory markers in the periodontium are detectable in the gingival crevicular fluid (GCF). GCF production fluctuates due to various factors. Our study aimed to assess the effect of tooth clenching or grinding on GCF volume and proinflammatory IL-1β concentration in GCF. This pilot study was carried out on 20 participants aged 21 to 28 with good general health (per 10 people studied and control groups). GCF volume was measured with Periotron 8010 after absorbing for 30 s with PerioPaper strips. Twelve samples were collected from each patient—the buccal and lingual surfaces of teeth 16, 11, 24, 36, 31, and 44 were included. Laboratory examination of IL-1β concentration was performed. In patients with pathological tooth wear, a tendency to increase GCF secretion and IL-1β concentration in GCF was found. GCF volumes were higher in posterior teeth, while IL-1β levels were higher in anterior teeth. Crevices at the molars seem to have a potential predictive value in diagnosing periodontal microinflammation in patients with probable bruxism. Due to occlusal overload, these bruxists are more prone to microinflammatory processes in the periodontium. Further studies in a broader group are required to confirm this correlation.

Enhanced neutrophil apoptosis accompanying myeloperoxidase release during hemodialysis

Biocompatibility of hemodialysis (HD) systems have been considerably improved. However, mortality and morbidity rates of patients have remained high, raising questions regarding the biocompatibility of current systems. In the present study, 70 patients on regular HD (51 males; mean age, 63 years; median duration of HD, 18 months) with high-performance membrane (polysulfone, 77%; polymethylmethacrylate, 23%) at Tohoku University Hospital were examined. Blood samples before and after HD, were subjected to measure apoptosis cells of white blood cells, plasma levels of the following molecules: myeloperoxidase (MPO), pentraxin 3 (PTX3), angiogenin, complements, and 17 cytokines. The main findings were as follows: significant decreases in leukocyte counts by dialysis, significant increases in apoptosis-positive leukocytes by dialysis (neutrophils and monocytes), and significant decrease in plasma angiogenin accompanying increase in plasma MPO and PTX3 levels, with no or only marginal changes in plasma pro-inflammatory cytokine levels and complement products by dialysis. The findings underlined the unsolved issue of bio-incompatibility of HD systems, and suggest the possible pathology of neutrophil apoptosis accompanying MPO release for the development of microinflammation in patients on HD.

Plasma lipopolysaccharide binding protein level statistically mediates between body mass index and chronic microinflammation in Japanese patients with type 1 diabetes.

Recently, it is widely recognized that microinflammation plays important roles in the pathophysiology of metabolic diseases, especially obesity-related disorders, diabetes and their complications. Lipopolysaccharide-binding protein (LBP) is a liver-derived acute-phase protein responsive to lipopolysaccharides (LPS) produced by gram-negative bacteria, thus reflects the systemic inflammation caused by the infection of those bacteria including gut dysbiosis. In this study, we evaluated the plasma LBP levels and investigated its clinical significance in 67 Japanese patients with type 1 diabetes. Univariable analysis showed that LBP levels were significantly associated with body mass index (BMI; r = 0.43, p < 0.01) and serum high-sensitivity C-reactive protein (hs-CRP; r = 0.64, p < 0.001) levels. However, there was no significant association between plasma LBP levels and diabetic complications. Mediation analysis revealed that LBP had significant mediation effects on the association between hs-CRP and BMI (0.27 [95% confidence interval 0.10-0.48]). These results suggest that the systemic condition where the LBP level increases, such as gut dysbiosis, at least partly, impacts onchronic microinflammation in patients with type 1 diabetes.

Study of Biocompatibility of Membranes in Online Hemodiafiltration

Background: The biocompatibility of dialysis membranes is a determining factor in avoiding chronic microinflammation in patients under haemodialysis. Lower biocompatibility has been related to increased inflammatory status, which is known to be associated with cardiovascular events. Classically, cellulose membranes have been considered bioincompatible. A new-generation of asymmetric cellulose triacetate (CTA) membranes allows the performance of high convective transport techniques, but there have been no studies of their biocompatibility. The aim of the present study was to analyze and compare the biocompatibility characteristics of 4 membranes, including CTA, in online hemodiafiltration (OL-HDF) patients. Methods: We included 15 patients in ­OL-HDF. After a 2-week washout period with helixone membrane, each patient was treated with the 4 membranes (polyamide, polynephron, helixone and CTA) for 4 weeks in a randomized order. The other dialysis parameters were kept stable throughout the study. We studied changes in markers of the activation of the complement system, monocytes, platelets, and adhesion molecules with the 4 membranes, as well as inflammatory parameters. Results: Biocompatibility was similar among the membranes. There were no sustained differences in complement activation, measured by C3a and C5a levels, or in platelet activation, determined by levels of P-selectin and platelet-derived microparticles (CD41a+). No differences were observed in activated monocyte levels (CD14+/CD16+) or in plasma levels of interleukin (IL)-1, IL-6, IL-10 or high-sensitivity C-reactive protein, although tumour necrosis factor-α levels decreased when the patients were dialyzed with CTA. No significant differences were found in markers of endothelial damage, assessed by levels of plasminogen activator inhibitor-1 and adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1). Conclusion: The 4 membranes evaluated in this study in stable patients on OL-HDF, including the new-generation CTA, show similar biocompatibility with the methods applied.

Clinical-functional features of the non-alcoholic fatty liver disease combined with metabolic syndrome depending on type of insulinemia and class of obesity

The aim was to evaluate the activity of liver enzymes, insulin resistance (IR) and micro-inflammation in patients with non-alcoholic fatty liver disease (NAFLD) and with metabolic syndrome (MS), depending on the type of insulinemia and the degree of obesity.Material and methods. The study involved 150 patients with NAFLD and MS. Depending on the level of endogenous insulin (EI) in the blood and the degree of obesity patients were divided into two groups: I group — 48 patients with normal level of EI in blood and normal body weight (BMI = 18–24,9 kg/m2); II group — 57 patients with spontaneous hyperinsulinemia (SH) and class I – III obesity (BMI&gt; 30,0 kg/m2). Control group — 20 practically healthy persons. The activity of alanine (ALT), aspartate aminotransferase (AST), total bilirubin, glucose, index of insulin sensitivity, ЕІ and ß2‑receptor of insulin, proinflammatory cytokine TNF-α, leptin cytokines and adiponectin levels were determined.Results. The HOMA-IR was significantly increased in both groups (p&lt;0,05). All patients showed a significant increase in insulin β2‑receptors. In patients with normal EI and with SH blood glucose levels, β2‑receptor levels in 3 and 5,5 times (p&lt;0,05), respectively, were significantly increased compared with control. In patients with spontaneous hyperinsulinemia it was 1,8 times higher than in patients with normal EI in blood and body weight (p&lt;0,05). Analyzing the levels of ALT and AST, it was found that in patients of Group I, the data varied within the control (p&gt;0,05), whereas in patients of Group II, ALT levels in 3 times exceeded control (p &lt;0,05) and in 2,8 times — the level in patients of Group I (p&lt;0,05) respectively; and the level of AST was greater in 1,5 times than in control (p&lt;0,05) and in in 2 times compared with Group I (p&lt;0,05). The level of leptin in patients with normal levels of EI in the blood and normal body mass exceeded this index in the control in 2,3 times (p&lt;0,05). In patients with SH and class I — III obesity — in 2,3 times compared with control group (p&lt;0,05), and in 2 times compared with patients of group І (p&lt;0,05). The level of TNF-α was significantly increased in all patients. In patients of Group I, this indicator exceeded the control level by 16,0% (p&lt;0,05). In patients of Group II, the TNF-α was greater compared with control group on 57,5%(p&lt;0,05) and on 57,5% compared with patients of Group І (p&lt;0,05). We have established hypoadiponectinemia in all patients with NAFLD in the background of MS, which was most pronounced in patients with spontaneous HI and class I — III obesity. In particular, in patients with normal levels of EI and normal body weight, the level of adiponectin was twice lower than in healthy persons (p&lt;0,05). In patients with spontaneous hyperinsulinemia and obesity, the adiponectin was in 2,8 times lower than in control (p&lt;0,05) and in 1,4 times compared with patients in Group I (p&lt;0,05). A direct correlations between spontaneous hyperinsulinemia, class I-III obesity and the level of leptin (r = 0,5381; p = 0,0001) were found.Conclusions. The features of NAFLD and MS are the severity of the course and the formation of IR with spontaneous hyperinsulinemia and class I – III obesity. It is characterized by an increase in the level of leptin, ß2‑receptors of insulin, activity of ALT, AST and hypoadiponectinemia.

Correlation between renal pelvic pressure and renal oxidative stress and microinflammation in ureteral lithotripsy

Objective To investigate the effects of ureteral pressure changes on oxidative stress and microinflammation in patients with ureteral lithotripsy. Methods From December 2016 to January 2018, 100 patients with renal calculi underwent ureteroscopic lithotripsy were treated in hospital. The ureteral pressure was monitored during operation. The patients with intraoperative ureteral pressure≥40 cmHg and cumulative time≥10 min were used as the high pressure group. The other patients were used as the low-pressure group. The urine microalbumin, urinary β2-microglobulin level, serum high-sensitivity C-reactive protein, interleukin-6, superoxide dismutase, malondialdehyde, glutathione level were measured before and at 1, 3, 5, and 7 days after operation. Results The blood pressure and heart rate of the two groups were not obvious after operation(P>0.05). The levels of urinary microalbumin, urinary β2-microglobulin, serum high-sensitivity C-reactive protein and interleukin-6 malondialdehyde were significantly increased (P<0.05), but the high-pressure group was in-creased higher significantly (P<0.05), superoxide dismutase and glutathione were significantly lower (P<0.05), and the high pressure group was more significantly (P<0.05). Pearson correlation analysis showed that renal pelvic pressure was positively correlated with urinary β2-microglobulin, serum high-sensitivity C-reactive protein, and malondialdehyde (r=0.716, 0.654, 0.632, P<0.05), and superoxide dismutase. There was a significant negative correlation with glutathione (r=-0.702, -0.711, P<0.05). Conclusions In patients with ureteroscopic lithotripsy, renal pelvic hypertension leads to renal dysfunction, inflammation and redox imbalance. Intraoperative control of renal pelvic pressure is beneficial to restore renal function and avoid further damage to renal function. Key words: Lithotripsy, Laser; Oxidative Stress; Inflammation

The relationship between urine neutrophil gelatinase-associated lipocalin and microinflammation in patients with hypertensive nephropathy

Objective To investigate the variation of urine neutrophil gelatinase-associated lipocalin (NGAL) level in hypertensive with early renal injury, and its relationship with micro-inflammation. Methods One hundred and seven patients with primary hypertension were recruited in this study. According to the level of urinary albumin excreting rate(UAER), these 107 patients were divided into three subgroups: 30 patients in normal albumin (NA) level in urine, 39 patients in micro albumin(MA)level in urine and 38 patients in clinical albuminuria(CA) . Another 40 healthy adults were recruited in this study as control group. Each patient’s testing results of NGAL and hypersensitive C-reactive protein(hsCRP) were recorded. The level of serum Cr was also recorded, the value of estimated glomerular filtration rate (eGFR) was calculated according to the formula of Cockroff-Gault. Results The level of urine NGAL in patients with hypertension was obviously higher than in control group with healthy adults (P<0.01). Furthermore, the difference of NGAL could be seen inside the group of hypertension: the level of urine NGAL in subgroup of MA and subgroup of CA was significant higher than in subgroup of NA (P<0.01). Additionally, the level of urine NGAL was negative correlation to eGFR (r=-0.403, P<0.01), and positive to serum hsCRP (r=0.451, P<0.01). Conclusions The level of urine NGAL increases obviously in patients with hypertensive nephropathy, and a positive correlation exists between the severity degree of renal injury and inflammation factor. It imply that the level of NGAL can be served as a tool for diagnosis of early renal injury and micro-inflammation in patients with hypertensive nephropathy. Key words: Hypertension; Kidney Diseases; Lipocalins; Inflammation

Functional Bowel Disease.

Introduction: Combination of Rome III criteria have a moderate accuracy for diagnosis of Irritable bowel syndrome (IBS). Colonoscopies are performed to rule out other etiologies, and >50% are normal being considered as a “functional disease”. It has been described and impaired intestinal barrier function with mucosal inflammation in the small bowel of this patients, and recent reports evidence a possible organic disease. However, this fact has not been completely evaluated. Aim: to determine utility of Confocal Laser Endomicroscopy (p-CLE) identifying colorectal mucosa micro-inflammation in patients with IBS. Methods: Prospective, controlled, non-randomized and simple blind study (Jan-2016/Mar-2017), including patients with IBS according to Roma III criteria (IBS group), and healthy patients (control group). Exclusion criteria: patients receiving NSAIDs, corticosteroids or antibiotics, heart, kidney, liver or severe metabolic disease, IBD, bacterial overgrowth, gastrointestinal bleeding, history of colitis, colonic obstruction, colectomy, allergy to fluorescein, pregnancy and poor bowel preparation (Boston Scale<6). Both groups underwent colonoscopy using p-CLE with target-biopsy of each colorectal section. Altered crypt architecture, epithelial gaps with fluorescein leaks and dilated and prominent branching vessels were the considered p-CLE criterion for inflammation. Following Geboes Scale, biopsies where evaluated by an only pathologist blinded to endoscopic findings. Overall diagnostic accuracy was defined by sensitivity, specificity, PPV, NPV, observed and inter-rater agreement. Results: A total of 444 biopsies (74 patients) were included (mean age 53.1 [25-90] yo, 64.9% women). Normal colonoscopy was observed in all cases. There were an increased number of inflammatory lesions at p-CLE in IBS group (65.8%) compared with controls (23.4%) (OR 6.28; 4.14 - 9.52; P<0.01) (table 1). Goebes' grade >0 was more frequently in IBS group (60.8 vs. 27.5%; P<0.01). p-CLE for inflammatory findings in IBS, considering target biopsy as gold standard, reached a sensitivity, specificity, PPV, NPV, observed and inter-rater agreement of 86.7, 88.7, 85.9, 89.4, 87.8 and 75.4%. Conclusion: p-CLE proved to be a reliable method for detecting colorectal mucosa micro-inflammation in patients with IBS, showing that patients with IBS have 6 times more prevalence of mucosal colorectal microinflammatory than healthy patients.Inflammatory lesions at p-CLE, n (%)

Multi-glycoside of Tripterygium wilfordii Hook.f. attenuates glomerulosclerosis in a rat model of diabetic nephropathy by exerting anti-microinflammatory effects without affecting hyperglycemia.

Multi-glycoside of Tripterygium wilfordii Hook. f. (GTW) has been proven to be clinically effective in relieving microinflammation in patients with early diabetic nephropathy (DN). However, the therapeutic mechanisms involved in vivo remain unclear. In the process of early DN, microinflammation and activation of p38 mitogen-activated protein kinase (MAPK) and canonical nuclear factor (NF)-κB signaling pathways are the important mechanisms by which hyperglycemia contributes to glomerulosclerosis (GS). Therefore, this study aimed to examine the ameliorative effects of GTW on GS, and then to clarify its anti-microinflammatory mechanisms by inhibiting p38 MAPK and NF-κB signaling activities in the kidney. All rats were divided into 4 groups: the sham group, the sham + GTW group, the vehicle group and the GTW group. The suitable dose of GTW and vehicle were daily administered for 8 weeks after the induction of DN by unilateral nephrectomy combined with intraperitoneal injections of streptozotocin (STZ). The general status of the rats, biochemical parameters, renal histological changes and macrophages in glomeruli, as well as expression of the key proteins in the p38 MAPK and canonical NF-κB signaling pathways and inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and transforming growth factor (TGF)-β1 in the kidney were examined, respectively. The results revealed that, GTW improved the general cond ition and biochemical parameters of the rats, but did not lower blood glucose; GTW attenuated GS and suppressed glomerular microinflammation including the infiltration of ED1+ cells in glomeruli and the protein overexpression of TNF-α, IL-1β and TGF-β1 in the kidney; GTW inhibited the protein overexpression of key signaling molecules of p38 MAPK and canonical NF-κB pathways in the kidney including phosphorylated p38 MAPK, phosphorylated inhibitor protein IκB and NF-κB (p65). On the whole, we expounded that GTW, as a natural regulator in vivo, alleviates GS without affecting hyperglycemia, by exerting anti-microinflammatory effects, including reducing macrophage infiltration in glomeruli, suppressing TNF-α, IL-1β and TGF-β1 overexpression in the kidney and inhibiting p38 MAPK and NF-κB signaling activities.

Turnover of type III collagen reflects disease severity and is associated with progression and microinflammation in patients with IgA nephropathy.

Renal fibrosis is the hallmark of progression to end-stage kidney disease. Non-invasive biomarkers of renal fibrosis could serve as specific end points in clinical trials and improve monitoring and stratification of patients with chronic kidney disease (CKD). To address this, we measured markers of collagen type III turnover in urine and serum of IgA nephropathy (IgAN) patients. We measured the collagen type III pro-peptide (Pro-C3), representing production, and a neo-epitope fragment (C3M), representing a specific degradation fragment of collagen type III, in urine and serum samples from two cohorts of IgAN patients using newly developed enzyme-linked immunosorbent assays. With increasing CKD stage, urinary C3M gradually decreased (mean C3M/creatinine: 17.3 ng/mg in CKD stage 1, 3.5 ng/mg in CKD stage 5) whereas urinary Pro-C3 gradually increased (mean Pro-C3/creatinine: 4.1 ng/mg in CKD stage 1, 20.8 ng/mg in CKD stage 5). The urinary Pro-C3/C3M ratio, a measure of collagen type III turnover, significantly increased in advanced CKD stages. Serum C3M was not related to CKD stage but was associated with microinflammation. Urinary C3M was significantly lower in patients whose CKD stage subsequently progressed compared with those who did not progress. Our results suggest that the combination of urinary markers of collagen type III turnover, in particular the urinary Pro-C3/C3M ratio, is a potential novel, non-invasive diagnostic and prognostic tool to specifically monitor extracellular matrix (ECM) remodelling in kidney fibrosis.

The odontogenic-related microinflammation in patients with chronic kidney disease

Objectives: This study estimated plasma levels of interleukin IL-1β, IL-6, tumour necrosis factor-α (TNF-α), interferon-γ (INF-γ) in chronic kidney disease (CKD) patients with a single odontogenic pathology. Material and methods: Forty-nine selected adult CKD patients with single odontogenic pathology based on clinical and X-ray examination: patients after proper root canal treatment, without periapical lesions (n = 12), with pulp necrosis (n = 7), with asymptomatic periapical lesions (n = 22), with periodontal disease (n = 8), and 14 with healthy teeth were enrolled. Patients with coexisting different dental pathologies and the evidence of other infection were excluded. In all patients plasma concentrations of CRP, IL-1β, IL-6, TNF-α, and INF-γ were measured. Results: Patients with periodontitis were characterized by increased concentrations of IL-6 and TNF-α. Those with pulp necrosis had significantly more frequently serum CRP level over 2 mg/L and presented significantly elevated IL-6, but decreased TNF-α concentration than in the subjects with healthy teeth. In patients with periapical lesions and patients after root canal therapy, the concentrations of cytokines did not indicate for the systemic inflammation. Conclusions: Periodontitis and pulp necrosis are important sources of systemic microinflammation in CKD patients. Plasma concentrations of IL-6 and TNF-α appear to be more sensitive markers of odontogenic inflammation in CKD patients than CRP.

Proinflammatory CD14+CD16+ Monocytes are Associated with Microinflammation in Patients with Type 2 Diabetes Mellitus and Diabetic Nephropathy Uremia

Diabetic nephropathy (DN) is a major cause of type 2 diabetes mellitus (T2DM) mortality. Innate immunity has been shown to be closely associated with the occurrence and progression of T2DM-associated complications. In this study, we investigated the expression of Toll-like receptor 4 (TLR4) and CD14(+)CD16(+) monocytes in patients with T2DM and DN patients with uremia and TLR4 response to lipopolysaccharide (LPS), and to further explore the potential effects of inflammatory immune response in T2DM and DN uremia. Thirty DN patients with uremia, 28 T2DM patients, and 20 healthy volunteers were enrolled for the determination of CD14(+)CD16(+) fluorescence intensity and TLR4 expression on monocytes by using peripheral blood flow cytometry. Serum C-reactive protein (CRP) level was determined by using the immunoturbidimetry. Peripheral blood mononuclear cells (PBMCs) were isolated and stimulated with LPS for 24 h. monocytes were collected to detect NF-κB p65 and phosphorylated STAT5(p-STAT5) expressions by using Western blotting. Supernatants were sampled for the determination of interleukin-6 (IL-6) concentration by using ELISA. Compared to normal control, T2DM patients and DN uremic patients had a significantly higher CD14(+)CD16(+) fluorescence intensity, TLR4 expression, serum IL-6 and CRP level, whilst these biomarkers were more upregulated in DN uremic patients than in T2DM patients. Following the exposure to LPS, PBMCs showed a significant upregulation in NF-κB-p65 and p-STAT5 expression and a remarked increase in Supernatants IL-6 level, in a positive correlation with disease severity. Our results suggest that the disturbance in proinflammatory CD14(+)CD16(+) monocytes occurs in T2DM and DN uremic patients. Such immunological dysfunction may be related to the activation of TLR4/NF-κB and STAT5 signaling pathways underlying the immune abnormalities of CD14(+)CD16(+) monocytes.

ODONTOGENIC-RELATED MICRO INFLAMMATION IN PATIENTS WITH HYPERTENSION AND CHRONIC KIDNEY DISEASE: PP.15.78

Background: Micro-inflammation in patients with chronic kidney disease seems to be an important factor in the pathogenesis of accelerated atherosclerosis. The source of micro-inflammation usually left undetectable. Dental and peridental diseases may have important influence on micro-inflammation status in patients with chronic kidney disease (CKD). Aim of the study was to analyze concentration of selected inflammatory markers in CKD patients with potential dental and peridental diseases. Patients and Methods: Sixty eighty adult patients with arterial hypertension and stadium 1–4 of CKD were enrolled into the study. Based on clinical and X-ray examination patients were divided on 5 groups: group I (n = 12) - patients with teeth after endodontic treatment without periapical lesions, group II (n = 8) - patients with teeth with gangraena pulpae without periapical lesions, group III (n = 22) - patients with teeth with periapical lesions, group IV (n = 7) - patients with periodontal disease, and control group - with health teeth (n = 19). The evaluation was based on the Gingival Index (GI, scores 2 and 3) proposed by Löe and Silness, and the Russell's Periodontal Index (scores 6 and 8). Patients with multiple dental pathology and evidence of other then odontogenic infection were excluded from the study. In all patients serum hsCRP and hsIL-6 concentrations measured. Results: Similar concentration of serum CRP concentrations were observed in all studied groups [I-4.0(0.5–7.5)mg/L II-5.1(2.8–7.4)mg/L; III-3.7(1.8–5.5)mg/L; IV-3.2(1.6–4.8)mg/L; C-4.5(1.9–7.0)mg/L]. Significantly higher serum IL-6 concentrations were observed only in group II then in the control group [3.15(0.39–6.69) pg/mL vs. 0.91(0.63–1.18)pg/mL; p = 0.02, respectively]. Conclusions: 1. Serum concentration of hsIL-6 seems to be better than of CRP marker of periodontal-related inflammation in patients with chronic kidney disease. 2. The main source of periodontal-related inflammation is pulpal necrosis in patients with chronic kidney disease.

Odontogenic-related micro inflammation in patients with chronic kidney disease

Background and Objectives: Micro-inflammation in patients with chronic kidney disease seems to be an important factor in the pathogenesis of accelerated atherosclerosis. The source of micro-inflammation usually left undetectable. Dental and periodontal diseases may have important influence on micro-inflammation status in patients with chronic kidney disease.

Microinflammation in patients with Crohn's disease in clinical remission

Background and aims It is not clear whether Crohn's disease patients in clinical remission (Crohn's disease activity index < 150) display normal concentrations of inflammation sensitive biomarkers. Our goal in this work was to explore the intensity of the microinflammatory response in a group of Crohn's disease patients in clinical remission. Methods High sensitivity C-reactive protein, quantitative fibrinogen, erythrocyte sedimentation rate as well as platelet and leukocyte counts were examined in a group of 76 patients with Crohn's disease in remission and in 228 matched controls. Results Crohn's disease patients in clinical remission displayed a statistically significant ( p < 0.001) elevated concentration of hs-CRP (4.83 ± 3.8 mg/l) compared to controls (1.05 ± 2.9 mg/l). All other bio-markers were also significantly higher in Crohn's disease patients in remission compared to controls. Similar results were obtained in a subgroup of Crohn's disease patients with very low disease activity — CDAI < 75. Conclusions Clinical remission is not equivalent to biochemical remission raising a question concerning the true definition of remission in Crohn's disease.