, 1988). Notably, nonencapsulated pneumococci show more autolysis and release more pneumococcal RNA during growth than encapsulated pneumococci (Vered et al., 1988; Fernebro et al., 2004). Moreover, increased autolysis in nonencapsulated strains compared to encapsulated strains may even have underestimated the higher viable counts in our study. Secreted bacterial RNA fragments may impact pathogenesis (Obregon-Henao et al., 2012). The contribution PI3K Inhibitor Library of S. pneumoniae virulence factors

in host respiratory colonization and disease varies according to the in vivo location of the bacterium. In line with our findings, others described previously that nonencapsulated pneumococci possess increased resistance against cationic antimicrobial peptides compared to encapsulated pneumococci (Beiter et al., 2008). Pneumococcal resistance to extracellular neutrophil proteases may be of greater relative importance than inhibition of opsonophagocytosis on the mucosal surface in comparison with other body compartments such as the bloodstream or lung parenchyma. On the mucosal surface, phagocytosis may be ineffective, but neutrophil degranulation and release Opaganib concentration of toxic substances including neutrophil proteases may effectively kill pneumococci. However, definitive in vivo data demonstrating the contribution of extracellular killing of pneumococci are lacking (Coonrod

et al., 1987). We conclude that human neutrophil proteases elastase and cathepsin G are active against pneumococci in general; however, nonencapsulated pneumococci show increased resistance to extracellular human neutrophil protease-mediated check killing compared to encapsulated pneumococci. The mechanism of this increased resistance and the effect on human colonization and (mucosal) infection remain to be elucidated. The authors declare that no conflict of interest exists. “
“In June 2009, the National Institute of Allergy and Infectious Diseases (NIAID), Division of Allergy, Immunology

and Transplantation (DAIT), sponsored a workshop entitled Mast Cells in Innate and Adaptive Immunity. International experts in mast cell biology discussed recent advances in the field and future areas of research aimed at advancing our understanding of the importance of mast cells in shaping nonallergic, adaptive immunity to infection. Since 1954, the National Institutes of Health (NIH) has funded over 1000 grants related to mast cells 1. Of these, less than 10% have focused on mast cell responses to viruses, bacteria or helminths with the majority being directed to the study of mast cell mediators and allergic diseases. Thus, while the functions of mast cells in allergic diseases have been extensively studied, their role as effector cells against pathogens is poorly understood. The importance of mast cells for host defense is underscored by two observations: first, mast cells are found in lower organisms that developed several hundreds of million years ago, and second, no humans lacking mast cells have been described so far.

We postulate that the affinity of this mAb for the canine epitope is low, a view supported by a recent study in which a specific anti-canine CD25 this website mAb was developed in mice.55 A proportion of the ACT-1-negative cells may therefore be CD25+, which would reconcile this apparent anomaly with the observation that the majority of Foxp3/FOXP3+ T cells in both rodents and humans are CD25+. Stimulation of mononuclear cells derived from peripheral LNs with Con A for up to 120 hr elicited a significant increase in percentage and MFI of FOXP3 expression by both CD4+

and CD8+ T cells (Fig. 2). This phenomenon occurred in the absence of exogenous IL-2 or TGF-β, though the addition of low concentrations of IL-2 augmented CD25 and FOXP3 expression (Fig. 3a). Robust increases in CD25 expression were also observed in a recent study of CD4+ T cells derived from PB stimulated with Con A, yielding parallel increases in FOXP3 expression.64 However, similar experiments performed in an earlier study failed to elicit significant increases in the proportions of FOXP3+ CD4+ T cells without the addition of IL-2 and TGF-β,49 PS-341 manufacturer presumably reflecting differences in experimental conditions. Interestingly, in our study removal of the stimulus and continued culture disclosed a FOXP3high

population of lymphocytes that was IFN-γ− and predominantly CD4+ (Fig. 2d). Both the high level of FOXP383,84 and the lack of IFN-γ expression – Foxp3 directly represses the Ifng gene85,86 – suggested that this population was regulatory in nature, supported by our subsequent functional studies in vitro (Fig. 3d). Two alternative, non-mutually exclusive explanations for the increased proportion and absolute numbers of FOXP3+ T cells with polyclonal stimulation were considered – namely, up-regulation of FOXP3 in cells

that were originally either FOXP3intermediate or FOXP3−, or proliferation of pre-existing FOXP3+ T cells. The impressive increase in MFI of FOXP3 suggested that up-regulation of this molecule had occurred in individual cells, but parallel proliferation of pre-existing Treg cells could not be excluded. Reasoning that in both mice and humans Helios expression is restricted to nTreg cells and is not of induced by stimulation, even in the presence of TGF-β, we explored the expression of Helios in cells that had been stimulated in an identical manner to those for the functional studies. We observed an impressive increase in the number of FOXP3+ Helios+ cells with Con A stimulation, arguing for the proliferation of pre-existing nTreg cells. However, Helios expression was not limited to the FOXP3high population, which we speculated were Treg cells on the basis of their IFN-γ− phenotype in earlier studies (Fig. 2d).

Co-stimulation is not only relevant for the generation of effector T cell responses; several co-stimulatory molecules, including CD134 (OX-40), CTLA-4 and ICOS, have been indicated to also contribute to tolerance mechanisms mediated by Tregs[24,25]. CD137 expression has been found on Tregs and CD137 signalling has been shown to promote proliferation and survival of Tregsin vitro[26,27]. In a murine model of diabetes, treatment with anti-CD137 mAb increased Treg numbers significantly, which

mediated protective effects after adoptive transfer into non-obese diabetic–severe RG7204 combined immunodeficiency (NOD–SCID) recipients [17]. In contrast, other studies have pointed towards a negative effect of CD137 stimulation on Treg induction or activity. Choi

et al. demonstrated that CD137 signalling neutralizes the suppressive function of Tregsin vitro and in vivo[43]. Another study suggests that CD137 signalling is not important for Treg function, as Tregs isolated from CD137−/− mice prevented colitis pathology efficiently in a CD4+ T cell transfer model to SCID mice [44]. So far, the exact importance of the CD137/CD137L pathway for Treg function or generation of respiratory tolerance in vivo has not been studied. Therefore, we also investigated whether CD137 might play an immune regulatory role in vivo. CD137 deficiency had no impact on respiratory tolerance induction in our model, as CD137−/− mice were protected equally from the development of allergic parameters www.selleckchem.com/products/ABT-263.html compared to WT mice by mucosal antigen application prior to sensitization. We could not detect changes in Treg frequencies between WT and CD137−/− mice. Thus, the lack

of CD137 seems not to inhibit Treg development or function in our model. Taken together, our results demonstrate that loss of CD137/CD137L signalling neither affects the generation of Th2-mediated allergic airway inflammation nor influences the induction of respiratory tolerance Molecular motor in our murine model. While the current study investigated the role of CD137 in a murine model of allergic asthma, there are only limited data on CD137 function in the human system with regard to allergic, Th2-mediated immune responses: CD137 expression has been detected on eosinophils and associated with apoptosis of eosinophils [45]. Moreover, CD137 expression has been reported on T cells infiltrating the conjunctival stroma in patients with severe allergic conjunctivitis compared with controls [46]. Thus, future studies are required to elucidate the exact role of CD137 signalling in allergic diseases in humans. This study was supported by the German Research Foundation [Research Training Group GRK 1441 ‘Allergic response in lung and skin’; SFB 578 (TP14) ‘Immune reactions of the lung in infection and allergy’].

The authors would like to thank Ane M Rulykke for excellent technical assistance. We would like to thank Jesper Jurlander for sharing reagents and ideas. Anti-CD20 antibodies were a kind gift from Mark S. Cragg and Claude H.T. Chan, whom we would also like to thank for scientific discussions. We would like to thank Esben G. Schmidt for technical support and Morten Rasch for advice on protease inhibition. This work was made possible by the University of Copenhagen, Faculty of Health Sciences and The Neye Foundation. The authors declare to have no financial conflicts or interest. “
“Formation https://www.selleckchem.com/products/DAPT-GSI-IX.html of immune synapses (IS) between T cells and

APC requires multiple rearrangements in the actin cytoskeleton and selective receptor accumulation in supramolecular activation

clusters (SMAC). The inner cluster (central SMAC) contains the TCR/CD3 complex. The outer cluster (peripheral SMAC) contains the integrin LFA-1 and Talin. Molecular mechanisms selectively stabilizing receptors in the IS remained largely unknown. Here, we demonstrate that sustained LFA-1 clustering in the IS is a consequence of the combined activities of the actin-bundling protein L-plastin (LPL) and calmodulin. Thus, upon antigen-recognition of T cells, LPL accumulated predominantly in the peripheral SMAC. siRNA-mediated knock-down of LPL led to a failure of LFA-1 and Talin redistribution – however, not TCR/CD3 relocalization – into the IS. As a result of this LPL knock-down, the T-cell/APC interface became smaller over time and T-cell proliferation was inhibited. Importantly, Procaspase activation binding of calmodulin to LPL was required

for the maintenance of LPL in the IS and consequently inhibition of calmodulin also prevented stable accumulation of LFA-1 and Talin, but not CD3, in the IS. During the activation of T cells Phospholipase D1 the immune synapse (IS) is formed at the area of interaction between T cells and APC 1, 2. The IS is involved in enhancing, directing and terminating the T-cell immune response (for review, see 3–7). Within the IS, surface receptors as well as intracellular signaling and scaffolding proteins are organized in distinct structures, which are called supramolecular activation clusters (SMAC). The inner cluster (central SMAC or cSMAC) contains PKCΘ and the TCR/CD3 complex. The outer cluster (peripheral SMAC or pSMAC) is composed of the integrin LFA-1 (CD11a/CD18) and Talin 8. It is clear that for the development of an IS the actin cytoskeleton is of special importance 2, 9–11. For construction of an actin meshwork, as it is found in the IS, crosslinking and bundling of F-actin is indispensable to support F-actin rigidity. Here, we demonstrate that the actin-bundling protein L-plastin (LPL) is an important component to orchestrate the ordered formation of a mature IS. LPL is a leukocyte-specific protein.

We found that T. cruzi infection led to increased expression of PD-1 and its ligands on peritoneal Mφs as well as during in vitro infection. On the other hand, F4/80+ Mφs from T. cruzi-infected mice suppressed the proliferative response of naive CD90.2+ T cells to primary stimulation with Con A. The PD-L1 or PD-1 blockade significantly reduced the suppressive

activity of T. cruzi-infected-Mφs, indicating that PD-L1 is directly involved in their suppressive activity. However, PD-L2 blockade was not able to restore the T-cell proliferation suppressed by T. cruzi-infected Mφs. Given that it has been demonstrated that PD-L2 Volasertib datasheet KO mice show an increase in Th2 response,47,48 we decided to evaluate if PD-L2 blockade was able to induce Arg I. Involvement of Arg I in the suppressive AP24534 ic50 capacity of Mφs has been broadly demonstrated.26,27,60 Our data showed that PD-L2 blockade in T. cruzi-infected Mφs induced Arg I activity and expression that might explain the immunosuppressive capacity of these Mφs. However, we did not see changes in Arg I expression and activity in cell cultures treated with PD-1 or with PD-L1 blocking antibodies. Therefore,

in our T. cruzi infection model the immunosuppression may be directly mediated by PD-1/PD-L1 and indirectly by PD-L2 through Arg I regulation. Moreover, supporting data demonstrated that Arg I plays a key role in T-cell suppression in non-healing leishmaniasis lesions.26 Arg I, through the local depletion of l-arginine, impairs at the site of lesions the capacity of T cells to proliferate and to produce IFN-γ, which is required for parasite elimination.26 However, during Schistosoma mansoni infection, Arg I from Mφs favours the recovery of the infection by inhibiting T CD4+ cells and the production of cytokines.

The authors demonstrated Thymidine kinase that the primary suppressor mechanism was the depletion of arginine by Arg I from Mφs.60 Here, we show that PD-L2 blockade as well as PD-L2 deficiency enhances Arg, leading to an increase in parasite proliferation. In addition, Terrazas et al.38 have shown that Taenia crassiceps-induced Mφs were able to suppress T-cell proliferation through PD-L1 and PD-L2 up-regulation on Mφs in an IL-10, IFN-γ, NO independent and cell-to-cell contact dependent manner. In addition, Schistosoma mansoni worms selectively up-regulate PD-L1 to reduce T-cell activation during early acute stages of infection before the subsequent emergence of egg-induced T-cell suppression in the chronic stages of infection.61 Recently, It was shown that IL-4-stimulated Mφs up-regulate PD-L2 and the T-cell suppression induced by these Mφs was restored by adding anti-PD-L2 blocking antibodies.62 Therefore, T-cell suppression could be mediated by PD-L1 or PD-L2, depending on the manner in which Mφs are stimulated.

glabrata and C. albicans have not been formally evaluated in a diverse patient group.

We performed a retrospective study of adult inpatients from January 1, 2003 to April 30, 2008 with C. glabrata and C. albicans candidaemia at a single tertiary care centre in Detroit, Michigan to evaluate for differences in risk factors and presumed source of infection in these groups. Patients’ underlying conditions, risk factors and source of infection (probable or definite) were compared. Among 119 patients, 80 (67.2%) were C. albicans and 39 (32.8%) C. glabrata. Using logistic regression analysis, patients with C. glabrata infection were more likely to have diabetes mellitus (OR 2.43; 95% CI, 1.06–5.54) and abdominal source of infection (OR 4.53, 95% CI, 1.72–11.92). Mortality rates in the two groups were similar. Patients www.selleckchem.com/products/MLN-2238.html with C. glabrata candidaemia are more likely

to be diabetic and have an abdominal source of infection compared with patients with Metabolism inhibitor C. albicans. “
“The biological activity of crude extract and fractions of Hymenaea martiana was evaluated against a panel of human pathogenic fungi. The crude extracts and hydroalcoholic fractions (E) showed a high activity against Cryptococcus neoformans species complex isolates with MICs between 2 and 64 μg ml−1. The methanolic (C) and butanolic (D) fractions were the most active against Trichopyton rubrum, Trichopyton mentagrophytes and Microsporum canis with MICs between 8 and 256 μg ml−1. None of the extracts

was active against the yeast Malassezia furfur, Malassezia obtusa and Malassezia sympodialis. “
“Invasive aspergillosis (IA) is a major cause of morbidity and mortality in immunocompromised hosts. Economic expenditures prompted by this invasive fungal infection (IFI) are significant. Although, the duration and associated costs of hospitalization comprise the largest proportion of costs Meloxicam in large surveillance studies, the newer oral antifungal agents may impact significantly on these costs. A review of the pharmacoeconomic (PE) studies is provided focussing on primary therapy, salvage therapy, empiric therapy and prophylaxis for IA. PE evaluations have demonstrated the cost effectiveness and dominance of voriconazole for targeted primary treatment of IA compared with other available agents. Differences in the drug choice and analytic methodology of the PE analyses of empiric antifungal strategy hamper definitive conclusions about the agents employed as empiric antifungal that may be directed at suspected IA although both caspofungin and voriconazole appear to be cost effective and dominant over liposomal amphotericin B (LAmB), whereas LAmB is more costly than conventional amphotericin B. Posaconazole is the most cost-effective agent for antifungal prophylaxis against IFI and IA. “
“The strict nutritional requirements of Malassezia species make it difficult to test the antifungal susceptibility.

The origin seems multi-factorial, but to an important extent explainable by prednisolone action. Gene signatures in patients with AAV undergoing steroid treatment should therefore be interpreted accordingly. “
“The endotoxic activities of lipopolysaccharides (LPS) isolated from different strains of rhizobia and rhizobacteria (Bradyrhizobium, Mesorhizobium, and Azospirillum) were compared to those of Salmonella enterica sv. Typhimurium LPS. The biological activity of all the examined preparations, measured as Limulus lysate gelation, production of tumor necrosis factor (TNF), interleukin-1β (IL-1β),

and interleukin-6 (IL-6), and nitrogen oxide (NO) induction in human myelomonocytic cells (line THP-1), was considerably lower than that of the reference enterobacterial endotoxin. Among the rhizobial lipopolysaccharides, the activities of Mesorhizobium CHIR-99021 molecular weight huakuii and Azospirillum lipoferum LPSs were higher than those of the LPS preparations from five strains of Bradyrhizobium. The weak endotoxic activity of the examined preparations was

correlated with differences in lipid A structure compared to Salmonella. Soil bacteria belonging to the rhizobium lineage are able to fix atmospheric nitrogen during symbiosis with legume plants. Bacteria from the genus Bradyrhizobium induce nitrogen-fixing nodules on the roots of cultivated (Glycine max and Glycine soya) and wild-growing legumes (1, 2). M. huakuii induces the formation of nodules on the roots of Astragalus sinicus (3). A. lipoferum represents plant-growth-promoting rhizobacteria which colonize the root surface and are not able to penetrate root IMP dehydrogenase cells. They live in association selleck products with roots of grasses, cereals, and other monocotyledonous plants (4, 5). Lipopolysaccharide, as an integral component of the cell walls of Gram-negative bacteria, plays an essential role in the proper development of symbiotic relationships (6). LPS, together with Omp proteins, is responsible for the asymmetric structure and semi-permeability of outer membranes. This is important for the appropriate morphogenesis and functionality of bacteroids, endosymbiotic forms of rhizobia which perform nitrogen

fixation (7). LPS may play a role in the protection of rhizobia against plant defense response mechanisms. Suppression of systemic acquired resistance or hypersensitivity reaction has been shown during infection of plant tissues by microsymbionts (8–10). Most pathogenic bacteria possess LPSs displaying endotoxic activity against host organisms. Lipid A, the part of LPSs that anchors the whole macromolecule in the outer membrane, is the centre of endotoxicity. The fine structure of enterobacterial lipid A has been identified as a glycolipid comprised of a β-(1,6)-linked glucosaminyl disaccharide substituted by two phosphate groups at positions C-1 and C-4 and six fatty acid residues with two acyloxyacyl moieties with a distinct location (Fig. 1) (11, 15, 16).

“
“E. Colombo, S. Romaggi, F. Blasevich, M. Mora, C. Falcone, H. Lochmüller, L. Morandi and C. Farina (2012) Neuropathology and Applied Neurobiology38, 367–378 The neurotrophin receptor p75NTR is induced on mature myofibres in inflammatory myopathies and promotes myotube survival to inflammatory stress Aims:

Recent studies propose the neurotrophin receptor p75NTR as a marker for muscle satellite cells and a key regulator of regenerative processes after injury. Here, we investigated the contribution of cellular compartments other than satellite cells and regenerating myofibres to p75NTR signal in diseased skeletal muscle. Methods: We checked regulation of p75NTR expression in muscle biopsies from patients with inflammatory screening assay myopathies (polymyositis, dermatomyositis and inclusion body myositis), or

Becker muscular dystrophy, and in nonmyopathic tissues. Quantitative PCR, immunohistochemistry, immunofluorescence or electron microscopy were used. RNA interference approaches were applied to myotubes to explore p75NTR function. Results: We found p75NTR transcript and protein upregulation in all inflammatory myopathies but not in dystrophic muscle, suggesting a role for inflammatory mediators in induction of p75NTR expression. In inflamed muscle p75NTR was localized on distinct cell types, including immune cells check details and mature myofibres. In vitro assays on human myotubes confirmed that inflammatory factors such as IL-1 could induce p75NTR. Finally, RNA interference experiments in differentiated cells showed that, in the absence of p75NTR, myotubes were more susceptible to apoptosis when exposed to inflammatory stimuli. Verteporfin Conclusions: Our observations

that p75NTR is upregulated on skeletal myofibres in inflammatory myopathies in vivo and promotes resistance to inflammatory mediators in vitro suggest that neurotrophin signalling through p75NTR may mediate a tissue-protective response to inflammation in skeletal myofibres. “
“P301S MAPT transgenic mice (P301S mice) are a widely used model of frontotemporal dementia and parkinsonism linked to chromosome 17 with tau pathology (FTDP-17-tau). However, a systematic correlation between cognitive deficits and cellular tau pathology at different ages is still missing. Therefore, our study investigated memory deficits of P301S mice in relation to pathological tau species and dendritic spine pathology throughout adulthood. We analysed P301S mice behaviourally with the novel open field, rotarod, and Morris water maze tests to measure deficits in locomotion, balance and cognition, respectively; immunohistochemically with different tau antibodies for specific tau species; and with Golgi staining for dendritic spine pathology. We confirmed the occurrence of locomotor deficits at an age of 5 months and newly report memory deficits from 2.5 months of age onwards.

3,[73] which has been reported to destabilize nucleosomes.[74] A concomitant decline in H2A.Z was also observed at the promoter, particularly of the CD69 gene.[73] Enrichment of H2A.Z near the transcription start Angiogenesis inhibitor site and depletion concomitant with induction have also been reported for other inducible genes,[55, 75] the suggestion being that

incorporation of H2A.Z decreases the stability of the nucleosome. Complex programmes of transcriptional regulation orchestrate the carefully co-ordinated expression of signature immune-responsive genes in response to T-cell activation. The molecular switches that mediate such precise and intricate control have been best characterized for the key T-cell cytokine, IL-2. Given its cell-specific expression, rapid transcription response and importance in T-cell biology, IL2 is considered as a model gene for unravelling epigenetic switches. As summarized in Fig. 3, extensive analysis of the IL2 gene allows us to put forward a model of the complex multilayered hierarchy of gene regulatory processes that are likely to drive immune-responsive genes. In resting T cells, when no IL2 transcription occurs, the IL2 gene exhibits low levels of chromatin accessibility and is decorated by H3/H2A.Z mTOR inhibitor nucleosomes

with H2A.Z flanking its transcription start site.[66, 73] Moreover, silent IL2 transcription is reinforced by the repressive activity of the microRNA, mir-200c and transcription factor, Zeb-1.[21] Chromatin remodelling accompanies high levels of IL2 transcription in activated T cells and histone variant exchange takes place in the promoter regions with a loss of histone H3 and a gain of H3.3. In addition, a concomitant decline of H2A.Z levels accompanied gene induction. H3.3 carries active histone post-translational modifications such as K9ac across the IL2 gene.[73] The accessible chromatin state across the IL2 promoter in activated BCKDHB T cells exposes the binding sites for transcription

factors such as c-Rel for chromatin remodelling and Pol II to initiate IL2 expression.[48, 66, 76, 77] Transcription of IL2 is dependent on the formation of the active transcription complex with PKCθ, MSK1 and LSD1 as well as the adapter protein 14-3-3ζ with Pol II[21] and increase in the elongation marker H3K36me3.[48] Overall, as illustrated in Fig. 3, IL2 regulation perfectly depicts the multi-layered process from all levels of the chromatin, ranging from chromatin accessibility, histone modifications, microRNAs and transcription factors. This holds particular significance in T-cell biology as the level of IL2 dictates the outcome of the T-cell immune response. In summary, to understand the multi-layered process of transcriptional regulation, it is necessary to combine research from the systematic approach of bioinformatics and bench top experiments.

We compared the 7-year all-cause and cardiovascular mortality of the subjects with albuminuria (albumin-creatinine ratio ≥ 30 mg/gCr), proteinuria (≥ ±) and (≥ 1+) by dipstick. Results: The prevalence of the subjects with albuminuria, proteinuria (≥ ±) and (≥ 1+) were 14.9%, 8.4% and 4.4%, respectively. During the follow-up period (median 6.4 years), the all-cause and cardiovascular Decitabine cell line mortality was 4.0% (138 subjects) and 1.2% (41 subjects), respectively in the total population. In Kaplan-Meier analysis, the all-cause mortality of the subjects with albuminuria (7.4%), proteinuria (≥ ±) (7.2%) and (≥ 1+) (9.3%) were significantly higher than those of the counterparts without urinary

abnormality. In Cox-proportional analyses with the adjustment for possible confounders, albuminuria, but not dipstick proteinuria was an independent www.selleckchem.com/products/Rapamycin.html factor for the all-cause and cardiovascular mortality. In subgroup analyses, the hazard ratio of albuminuria was high, especially in the diabetic and non-hypertensive population. Conclusion: Albuminuria showed a higher

predictive ability for the all-cause and cardiovascular mortality than dipstick proteinuria in the Japanese community-based population. MATHEWS SHARON, T1, VIJAYAN MADHUSUDAN2, VEERAPPAN ILANGOVAN1, REVATHY LAKSHMI2,3, T THYAGARAJAN2, MATHEW MILLY1,2,3, ABRAHAM GEORGI1,2,3 1Pondicherry Institute Of Medical Sciences; 2Madras Medical Mission; 3Tanker Introduction: Hydration

and nutritional status of end stage renal disease(ESRD) patients are linked to increased morbidity and mortality. Body composition monitoring (BCM) by Multi frequency Bioimpedance spectroscopy (MFBS) is considered to be a superior modality of fluid assessment in CKD–Dialysis. 3-mercaptopyruvate sulfurtransferase We did a longitudinal prospective study in south India on maintenance haemodialysis(MHD) and continuous ambulatory peritoneal dialysis(CAPD) patients over 24 months and looked at impact of baseline nutritional parameters and body composition parameters on 24 month mortality. Methods: Ninety nine patients stable on dialysis for at least 3 months were recruited (MHD 85, CAPD 14) at baseline and at 24 months, 41 were alive and 33 died, 12 underwent renal transplant and 13 were lost to follow up. BCM and nutritional assessment were done at baseline and at follow up. Results: Baseline overhydration differed significantly between surviving and dead patients (p < 0.05). Receiver operating characteristic(ROC) curve between overhydration and mortality showed area under the curve was >50% with best cut-off point to predict mortality as 3.15 L. ROC curve for BMI showed cut off of 22.65 kg/m2 to predict mortality, with sensitivity 41.30 % and specificity 81.81 %. At follow up, triceps skin fold thickness(TSF), biceps skin fold thickness(BSF) and mid arm circumference(MAC) increased significantly from baseline (p < 0.001, p= 0.001 and p.