but can be applied to other helminths and may contribute significantly to vaccine development against parasitic diseases in general. Bearing in mind the considerable potential of schistosomula as a source of effective vaccine antigens, techniques that overcome the difficulties of working with this developmental stage are required. One such

method, termed the ‘ASC-probe technique’ click here developed by Meeusen and Brandon (69,70), is particularly amenable to studying migrating larval helminths and has been used in a number of infections (70–76). In this technique, cells obtained from lymph nodes draining a particular infection site are cultured, which allows the in vivo-primed ASCs to secrete antibodies into the culture media. These antibodies,

present in the culture supernatants (ASC-probes), are specific for the pathogen infecting that tissue region and are only present in an active infection. ASC-probes obtained from lymph nodes draining different tissues from the same animal were shown to produce antibodies that can recognize distinct stage-specific antigens (70). Hence, these ASC probes can be considered to be a snapshot of the local antibody response, which is specific for (i) the tissue region, and (ii) the developmental stage of the pathogen within that tissue region. These tissue-specific ASC probes can be used for the discovery of their PI3K inhibitor target antigens and can therefore be considered to be a more IMP dehydrogenase relevant and directed tool for immunomic analysis compared to the complexity and nonspecificity of serum antibody probes. The ASC-probe technique was used to identify a surface antigen specific to the infective larval stage of H. contortus (termed Hc-sL3) (71), which was later found to be protective in a vaccine

trial (25). In this study, ASC-probes were produced from the lymph nodes draining the abomasum, the site of parasite infection, during the rejection response and identified by Western blotting an antigenic region at 70–83 kDa, which localizes to the larval surface (71). Because the ASC-probe response profile was much simpler than that obtained with immune serum, it enabled a more manageable and targeted approach for larval-specific antigen identification. Similarly, Jungersen et al. (73) and Meeusen and Brandon (70) used the technique to show that particular larval-specific antigens are recognized in distinct tissue compartments during Ascaris suum and Fasciola hepatica migration, respectively. Once again, antibodies against these antigens were not always detectable in serum. For schistosomes, as for other pathogens, antigen identification has long been performed using serum antibodies obtained from infected individuals and has enabled the discovery of various candidates (see Table 1) that are often the most immunogenic (27).

, 2004; Rehaume et al., 2010). Very little is known regarding the pathways regulating IL-17 when encountering pathogenic microorganisms, because only artificial

conditions, such as inducing TH17 proliferation with anti-CD3/anti-CD28, have been used. A recent work identified mannose receptors as the most important pathway for IL-17 induction and TLR2/dectin-1 as having a secondary amplification effect on mannose receptor-induced IL-17 production in response to C. albicans (Van de Veerdonk et al., 2009). A study by our group (Moresco et al., 2002) demonstrated that suckling mice pretreated with concanavalin-A (Con-A) survived an intraperitoneal inoculum of 5 × 107 C.  albicans, whereas all control selleck compound mice died within 24–48 h of infection. This effect of Con-A was attributed to IFN-γ production by direct bind to CD3 and TCR on T helper cells and subsequent increase in phagocytic and candidacidal activities of macrophages. On the other hand, IL-12 is a cytokine with links to both Ku-0059436 manufacturer innate and adaptative immunity systems, and it constitutes an essential component of the adaptative response that leads to the generation of Th1-type cytokine responses such as IFN-γ and TNF-α (Hamza et al., 2010) and protection against disseminated candidiasis (Ashman et al., 2010).

Previously, our group reported that treatment with Con-A for 3 days protected 100% of mice against a lethal inoculum of C. albicans by increasing activity of mannose receptors on peritoneal macrophages, which produced significantly more TNF-α and were more able to kill C. albicans in vitro or over the course of infection with Candida compared to

the control group (Conchon-Costa et al., 2007; Geraldino Vorinostat price et al., 2010). This study tested the hypothesis that greater activity of mannose receptors and dectin-1 on peritoneal macrophages from mice pretreated with Con-A could facilitate the activation of TH1 and TH17 subsets over the course of infection by C. albicans. Candida albicans strain CR15 was isolated from the oral mucosa of a patient with HIV infection at the university hospital and maintained on Sabouraud dextrose agar; the isolate was used after two serial animal passages. C. albicans blastoconidia were obtained by growth in Sabouraud dextrose broth for 24 h at 28 °C, were washed with phosphate-buffered saline (PBS) and resuspended at 107 blastoconidia in 1 mL of RPMI 1640 (Sigma-Aldrich, St. Louis, MO). Subgroups of five male Swiss mice, each weighing 28–32 g and aged 4–6 week old, received sterilized food and water ad libitum. The mice were pretreated with 250 μg of Con-A (Sigma-Aldrich)/250 μL PBS intraperitoneally (i.p.) or 250 μL PBS alone and 3 days later were infected with 1 mL of C. albicans CR15 107 (i.p.). One group of five noninfected mice was used as control.

Patients, who are mainly children, suffer from bloody diarrhea, recurrences are uncommon and their prognoses are often good 1. The other form, called atypical hemolytic uremic syndrome (aHUS), occurs at any age, may be sporadic or familial and has a poor prognosis as approximately 50% of the patients progress to end-stage renal disease PF-02341066 nmr and 25% die during the acute phase of the disease. The sporadic form of aHUS may be triggered by non-enteric infections, viruses, pregnancy, drugs, malignancies or transplantation

2. The familial form of aHUS has now been shown to be associated with genetic abnormalities in complement regulators like factor H (FH) 3–6, factor I (FI) 4, 7–10, membrane cofactor protein (MCP) 4, 11–14, C4b-binding protein (C4BP) 15, factor B (FB) 16 and C3 17 or autoantibodies against FH 18, 19. The mutations and polymorphisms in these proteins are mostly found in heterozygous form and can affect both the secretion and function of the proteins, leading to impaired regulation of the alternative pathway of the complement system 2. Since many of the patients carry several HDAC activity assay heterozygous mutations or polymorphisms in different genes, it has been suggested that a combination

of several simultaneous hits strongly predisposes to aHUS 20. The complement system, which is a part of the innate immune system, can be activated through three different pathways, the classical, lectin and alternative pathways. The classical pathway is initiated through the interaction of C1 with ligands such as immune complexes. The lectin pathway is initiated when mannose-binding lectin binds to carbohydrate structures on bacteria, whereas the alternative pathway is constantly activated through auto-hydrolysis of

C3 molecules in the fluid phase. Furthermore, the alternative pathway serves as the amplification loop to the other two pathways. All three pathways generate C3 convertases (C4b2a or C3bBb), which cleave C3 to C3a and C3b 21. To prevent activation by self-tissue, complement has to be tightly regulated by membrane-bound (MCP, decay-accelerating factor, complement receptor 1 (CR1)) and fluid-phase inhibitors (C4BP, FH, FI). Among these during inhibitors, the serine protease (SP) FI is special since it degrades C4b and C3b in the presence of specific cofactors like C4BP 22, FH 23, MCP 24 or CR1 25. FI is a unique protease since it has no natural inhibitors and works only together with its cofactors. The fully processed FI protein consists of a heavy chain (50 kDa) and a light chain (38 kDa), which are connected covalently via a disulfide bond 26. The heavy chain is composed of five domains; the factor I membrane attack complex (FIMAC), CD5-like domain, the low-density lipoprotein receptor 1 and 2 domains (LDLr1 and 2) and a region of unknown homology. The light chain comprises the SP domain 27.

Glucocorticoids are the sole drugs of clinical interest for DMD patients.

The mechanism for their beneficial action is not completely understood yet and may involve multiple effects, beside the classical anti-inflammatory and immunosuppressive ones. These include an improvement of regeneration and an increased expression of utrophin, the homologue-surrogate for dystrophin [20–22]. However, the clinical use of glucocorticoids in DMD children is limited by severe side effects over long-term use; this compels the search of safer drugs or of strategies to limit their side selleck screening library toxicity [23]. As for other complex disorders, one feasible strategy is to find compounds with relevant synergistic interactions: thus glucocorticoids in combination with a synergistic drug, may exert greater effects and/or have less side effects as a result of dose lowering. This rationale is reinforced by the anecdotal report that DMD patients often take various food and drink supplements or herbal remedies along with the classical glucocorticoids and it is important

to develop a more systematic preclinical evaluation of the outcome of drug combinations, both in vitro and in vivo[23,24]. For instance, the combination of deflazacort with the food supplement L-arginine has been reported to produce an improved functional benefit in dystrophic mdx Maraviroc cost mice [25]. We therefore aimed to investigate the effects of a combined treatment of α-methyl-prednisolone (PDN), a clinically used glucocorticoid, with taurine. Taurine is a sulphonic amino acid normally present in skeletal muscle, able to modulate sarcolemmal excitability and calcium homeostasis [26]. It is used as a soft-drink supplement for its claimed ability to stimulate metabolism and provide energy. Little, if any, toxicity has been reported for taurine

at the generally assumed quantities [27]. Complex next fluctuations in tissue taurine content occur in mdx mouse in the different phases of muscle degeneration/regeneration, suggesting that the amino acid levels may be influenced by myofibre state and may in turn contribute to cellular and tissue dysfunction and/or repair; taurine increases seem to be generally associated with muscle regeneration and membrane stabilization [28–30]. In addition, taurine exerts anti-inflammatory and antioxidant actions [31], with potential beneficial outcomes on the pathology progression. We have previously found that taurine either applied in vitro or administered in vivo exerts beneficial effects on the altered excitation-contraction coupling mechanism of mdx myofibres [8,29]. Also the amino acid administration enhances mdx mouse strength impaired by a chronic exercise on treadmill, a protocol that is able to exacerbate in vivo and ex vivo markers of the murine pathology [2,8]. We have performed a chronic (4–8 weeks treatment) in vivo treatment with α-methyl-prednisolone (1 mg/kg i.p.

[55] Leukotrienes are synthesized in response to a large spectrum of various infectious agents and enhance the capacity of macrophages and other immune cells to ingest and kill microbes and to produce antimicrobial mediators. In animal models of infection, genetic or pharmacological interference with leukotriene synthesis or signalling massively impairs local microbial clearance.[56] In summary,

these data imply that ABT-737 mouse certain levels of leukotrienes are indispensable to control microbial invaders and to maintain local immune reactivity not only in the lung but also in the gastrointestinal tract. Similar to prostanoids, the SCFA n-butyrate brings about interference with immune cell activation at key stages of immune cell activation inhibiting dendritic cell maturation and consequent T-cell actions. Previous studies demonstrated that pre-treatment of human peripheral blood mononuclear cells or monocytes as well as monocyte-derived dendritic cells with this agent resulted in a dose- and time-dependent down-regulation

of their capability to stimulate T-cell responses.[8, 9, 22, 56-61] Therefore, it is tempting to speculate that n-butyrate itself, or through induction of mediators like eicosanoids, may contribute to the generation of an anti-inflammatory immune responsiveness. As the presence of n-butyrate is largely restricted to the gastrointestinal tract and immunological all features of this region have striking similarities to the effects brought about by click here this physiologically occurring substance, further elucidation of the underlying principles appears

promising. There are several potential transcriptional regulatory elements in the promotor region of the COX-2 gene including a peroxisome proliferator response element, two cAMP response elements, a sterol response element, two NF-κB sites, an SP1 site, a CAAT enhancer binding protein motif, two AP-2 sites, an E-box, and a Tata box.[63] Previous studies have shown that cAMP response element-binding protein (CREB) and NF-κB are particularly important in LPS-induced COX-2 transcription indicating that p65/p50 heterodimer together with CREB is required for an early phase of rapid induction and the p50 homodimer together with CREB is crucial during later phases.[63] Testing the impact of n-butyrate treatment on LPS triggering, we found that the early phase of NF-κB signalling including IκB phosphorylation, IκB degradation and phosphorylation of p65 and p50 was completely unaffected. The late phase of the classical NF-κB pathway, as indicated by p65/p50 DNA binding, however, was profoundly inhibited. These finding are in agreement with previous studies[25, 64-66] showing inhibition of NF-κB signalling by n-butyrate. Furthermore, we were able to demonstrate that phosporylation of p105, the precursor for the formation of p50 homodimer, was also sustained.

In fact, one of the first autoimmune complications to be described in primary immune deficiency was the rheumatological disease that occurs in XLA [7]. While subjects with the hyper-IgM syndromes have recurrent opportunistic infections with Pneumocystis jiroveci and Cryptosporidium and for the X-linked version, a tendency to develop biliary tract disease [8,9], autoimmune complications are also common. These occur in both the X-linked and autosomal this website forms and include joint, bowel, liver and haematological disease. Table 2 outlines the most common autoimmune conditions in groups of subjects with the X-linked and the autosomal form of hyper-IgM syndrome due to mutations in the activation-induced

cytidine deaminase gene (AID). Characteristics of these defects are the development of IgM antibodies but not IgG or IgA, lack of response to T dependent antigens and an inability to develop memory B cells. For the X-linked form, loss of CD40L signals on dendritic cells and thymic epithelial cells also occurs, and potentially a loss of development of Tregs. Some or all of these molecular defects leads to an increased number of mature naive B cells, which express a high proportion of autoreactive antibodies. As for subjects with XLA, subjects with hyper-IgM syndromes have circulating B cells with autoimmune potential;

however, these are not new emigrant B cells but naive B cells, suggesting loss of peripheral tolerance. Alterations BGB324 in vivo in B cell receptor signalling pathways are also found in patients with defects in Toll-like receptor (TLR) signalling, such as interleukin-1 receptor-associated kinase 4 (IRAK-4), myeloid differentiation primary response gene 88 (MyD88) and unc-93 homologue B1 (UNC-93B) [10–12] for less clear reasons.

These observations demonstrate Cobimetinib molecular weight that B cell tolerance in humans normally relies upon a number of pathways working as an interactive network to exclude B cell autoimmunity. In CVID, B cells secrete immune globulins poorly, and fail to differentiate into plasma cells. About 25–30% of these subjects develop autoimmune complications; for unclear reasons, more than 50% of these involve the haematological system, with immune thrombocytopenia and haemolytic anaemia being foremost [13–17] (Table 3). While defects of single genes have helped to elucidate autoimmunity in selected primary immune defects, the cause of autoimmunity in CVID has proved more complex and a number of mechanisms are likely. Similar to the hyper-IgM syndrome, CVID B cells exhibit impaired somatic hypermutation [18], and there are reduced numbers of CD27+ memory B cells and an even greater losses of isotype-switched (IgD– IgM– CD27+) memory B cells [19]. Loss of these cells is associated with both the development of autoimmunity, lymphoid hyperplasia, splenomegaly and granulomatous disease [19–22] (Fig. 1 shows data for a Mount Sinai cohort).

Chaplains were well used in some services. Participants had received no pre and little in-service training or education in spiritual care. Suggestions for improvements included in-service

training, better utilization of chaplaincy services and training in advance care Talazoparib order planning. Most participants indicated they would attempt to provide some form of spiritual care, either directly or by referring the patient to appropriate services. However, participants generally demonstrated a lack of confidence in addressing a patient’s spiritual needs. “
“Rodent models of renal physiology and pathology are crucial to our understanding of the molecular, histological and functional sequelae that contribute to kidney diseases. One of the most important measures of renal function is glomerular filtration rate (GFR). Whilst the accurate determination of GFR is pivotal to understanding the progression of disease and/or the benefits of treatment strategies, Osimertinib in rodents the conventional methods for assessment of GFR are inconvenient and cumbersome, not the least because they involve stress and often, anaesthesia.

The legitimacy of assay-based assessment of plasma and urine markers of GFR in mice has also been heavily scrutinized for their insensitivity to minor declines in GFR and inaccurate detection of renal biomarkers. Whilst infusion-based clearance methods of GFR assessment are thus the gold standard in terms of accuracy, they are limited by the fact that they are primarily non-recovery procedures. This presents Methocarbamol a dilemma when trying to document the progression

of renal disease, as these measures cannot be taken in the same experimental subject. Here we review a technique of transcutaneous measurement of FITC-sinistrin to calculate GFR in small rodents, using a Non-Invasive Clearance Device (NIC-Kidney Device). This is a recently validated non-invasive technique for measuring GFR in small rodents that allows for the real time measurement of GFR in conscious animals, without the need for plasma and urine assays. “
“Background:  Vascular calcification (VC) contributes to cardiovascular disease in haemodialysis (HD) patients. Few controlled studies have addressed interventions to reduce VC but non-calcium-based phosphate binders may be beneficial. No published randomized study to date has assessed the effect of lanthanum carbonate (LC) on VC progression. Methods:  We conducted a pilot randomized controlled trial to determine the effect of LC on VC. Forty-five HD patients were randomized to either LC or calcium carbonate (CC). Primary outcome was change in aortic VC after 18 months. Secondary outcomes included superficial femoral artery (SFA) VC, bone mineral density (BMD) of lumbar spine and serum markers of mineral metabolism. At baseline, 6 and 18 month computed tomography was performed to measure VC and BMD. A random effect linear regression model was performed to assess differences.

Removal of these Selleck LY2835219 cells occurs rapidly and without induction of a proinflammatory milieu 1. In recent years, it has become apparent that the removal of apoptotic cells by macrophages and DC is not only noninflammatory but also immune-inhibitory 2–8, in most although not all circumstances. Fadok et al. 2 showed that efferocytosis (clearance of apoptotic cells, a terminology suggested by the Henson group) inhibited the production of proinflammatory

cytokines such as IL-8 and IL-1β, and induced the secretion of TGF-β, platelet-activating factor, and prostaglandin E2. They further showed and suggested that these factors inhibited a proinflammatory response to LPS and zymosan, by autocrine or paracrine mechanisms, via the secreted factors. Later, Huynh et al. 4 showed that the resolution of acute inflammation www.selleckchem.com/products/poziotinib-hm781-36b.html is dependent on phosphatidylserine expressed by apoptotic cells, and on TGF-β, secreted most probably by macrophages following engulfment of apoptotic cells expressing phosphatidylserine. Freire-de-Lima et al. 3 further showed

that through TGF-β, apoptotic cells simultaneously induce an anti-inflammatory milieu and suppress proinflammatory eicosanoid and NO synthesis in murine macrophages. Hence, the proposed model for inhibition of a proinflammatory response to LPS and zymosan, as well as the resolution of acute inflammation, is based on ligation of phosphatidylserine expressed on apoptotic Farnesyltransferase cells to the presumed phosphatidylserine receptor, and possibly other receptors. This ligation is expected to result in immediate preformed TGF-β secretion from macrophages, followed by de novo synthesis of TGF-β. Additional mechanisms of inflammatory response inhibition in humans have been proposed by other groups (reviewed by Serhan and Savill,

9). We have recently shown that thrombospondin-1 ligation to phagocytic cells 5 and STAT-1 inhibition 7 are additional inhibitory mechanisms. In some circumstances, clearance of apoptotic cells and necrotic cells can be proinflammatory, as a result, for example, of autoantibody-opsonization of apoptotic cells or release of proinflammatory molecules such as high mobility group box-1 protein (HMGB1) 10. We and others were also able to show that complement may be involved in apoptotic cell uptake via direct binding of bridging factors like C1q and mannose-binding lectin 11, or formation of iC3b on the surface of apoptotic cells 8, 12, 13. Thus, opsonization by complement and engagement of the complement receptors CD11b/CD18 and CD11c/CD18 may suggest an alternative or complementary clearance mechanism. Complement opsonization of bacteria was generally known for its proinflammatory effects.

This work was supported by Medical College of Georgia Intramural Scientist Training Program to N. S. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by MLN8237 clinical trial the authors.

“
“The autoimmune reaction is recently suspected to play a role in the pathogenesis of chronic obstructive lung disease (COPD). As COPD is a systemic disease, the elements of an autoimmune response in circulatory system is of interest. It has been shown that regulatory T cells are important in the control of autoimmunity. There are some data on a role of adiponectin in the regulation of immune reactions. The objective of this study was to assess the elements of autoimmune reaction in the peripheral blood (PB) of patients with COPD. Twenty-eight patients with mild/moderate COPD and 20 healthy volunteers learn more were investigated. Flow cytometry method with mixtures of monoclonal antibodies anti: CD14/CD45, CD3/CD19, CD4/CD25/CTLA4 and CD8/CD25 were used. Concentration of adiponectin was measured using ELISA method. We observed significantly lower proportion of CD4+/CD25+ as well as CD4+/CD25+ high

cells in COPD patients than in healthy controls (15.3 versus 17.8% and 0.79 versus 1.54%, respectively, P < 0.05). The proportion of CTLA4+ cells in CD25+ cells and

the mean fluorescence of CTLA4 on CD4+ buy Rucaparib cells were higher in patients than in healthy controls (10.4 versus 4.7%, P < 0.05, 189% versus 149%, non significant, respectively). We found significantly elevated concentration of adiponectin in patients when compared to healthy subjects (15.4 versus 8.5 μl/ml, P < 0.05). We found that the adiponectin/BMI ratio correlated with the decrease of FEV1%. The results of this study support the possible role of CD4/CD25/CTLA4 cells and adiponectin in the systemic inflammation in COPD. Chronic obstructive pulmonary disease (COPD) is a progressive disorder, characterized by poorly reversible airway obstruction and persistent inflammation in the lung tissue [1]. This disease affects mainly the respiratory tract. However, many data confirmed relevant systemic disturbances in course of COPD [2, 3, 4]. Up to date, the following pathways in systemic inflammation in COPD have been described: cytotoxic effect of CD8+ cells, elevated concentration of inflammatory cytokines, increased apoptosis of inflammatory cells and impaired resolution of inflammation [2, 3, 5–9]. There is evidence that activated lymphocytes play a crucial role in the pathogenesis and in the adaptive immune response in COPD [6]. Microbial peptide antigens are well known to be active in development of adaptive immunity [8]. However, recently some autoantigens were postulated to play important role in pathogenesis of COPD [10–12].

18G AUTOMATED NEEDLES   J Mai, A Aravindan, H Dickson, J Yong, M Suranyi, J Wong   228 URINARY TRACT INFECTIONS AT LIVERPOOL HOSPITAL   Z Hasan, M Maley, M Surany, J Wong   229 THE INFLUENCE OF DIETARY VITAMIN D INTAKE ON VITAMIN D STATUS IN CHRONIC KIDNEY DISEASE PATIENTS   E Murray, K Campbell, L Orazio, N Isbel, W Petchey   230 AGE AND SERUM CALCIUM ARE ASSOCIATED WITH INFRA-RENAL AORTIC CALCIFICATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE   R Dua, B Nguyen, K Sangla, J Golledge   231 VITAMIN D INSUFFICIENCY AND CHRONIC KIDNEY DISEASE IN AUSTRALIA: THE AUSDIAB STUDY   M Damasiewicz, D Magliano, R Daly, C Gagnon, Z Lu, P Ebeling,

S Chadban, R Atkins, P Kerr, J Shaw, K Polkinghorne 1300–1400 LUNCH & TRADE EXHIBITION  

Hall G 1400 ASM CONCLUDES “
“Aims:  The aims of this study is to correlate colour duplex ultrasonography (US) with contrast fistulography for the detection of functional stenoses in the XL765 autogenous AVF (arterio-venous fistula) circuit. Methodology:  Colour duplex US scans of 93 dialysis patients with dysfunctional this website AVF were compared with fistulograms performed within 6 weeks of the US. The AVF circuit was divided into six zones: inflow artery; anastomosis; distal vein; mid vein; proximal vein; and central vein. Colour duplex US and fistulogram images/reports were independently re-reported for stenoses in each fistula zone by two trained clinicians blinded to the outcomes. For each fistula, only zones examined by both modalities were included in the study. Kappa analysis of the results was performed to assess the accuracy of colour duplex US in the dysfunctional AVF circuit. Results:  Most AVF studied were radio-cephalic (59%) or brachio-cephalic (22%). Stenoses identified within the AV circuit in order

of frequency were: distal vein (41), mid vein (23), arterial (12), proximal vein (7) and anastomosis (3). The interval between US and fistulogram studies was 33 ± 29 days. Congruence of results between US and fistulograms ranged from 85% to 96%, depending on the zone examined. Kappa analysis of this US versus fistulogram data was also moderate to good, ranging from 0.72 and 0.91. Conclusions:  Colour duplex US provides an accurate L-NAME HCl diagnostic assessment of a dysfunctional autogneous AVF, and is an important planning tool for subsequent open or endovascular intervention. It is particularly accurate in the peri-anastomotic area of the fistula which harbours the majority of fistula problems. “
“Aim:  3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) may have an adjunctive effect on chronic inflammation and nutrition status in renal dialysis patients. Therefore, we performed a systematic review of randomized controlled trials to assess the effect of statins on chronic inflammation and nutrition status in dialysis patients.