As COX-2 expression crucially depends on p50 homodimer binding to distinct promotor sites,[19-21] this pathway might also be responsible for up-regulation of COX-2 expression under the conditions used in the present study. Further investigations will have to elucidate the exact molecular mechanisms leading to this potential converse effect of n-butyrate on different NF-κB signalling pathways. In conclusion, we have demonstrated AZD4547 mw that n-butyrate potently up-regulates expression of key enzymes and receptors of the eicosanoid pathway when activated via bacterial stimulation, leading to an increased release of PGE2, 15d-PGJ2,

LTB4 and thromboxane B2. Through selective induction of several eicosanoid mediators and up-regulation of its receptors we speculate that such effects of SCFAs might contribute to the generation of the gut intrinsic milieu, thereby specifically regulating the local gastrointestinal

immune response. Figure S2. n-Butyrate up-regulates cyclo-oxygenase 2 (COX-2) expression in monocytes after both Nutlin-3 cell line lipopolysaccharide (LPS) and Staphylococcus aureus cell (SAC) stimulation as demonstrated by Western blot. Results are representative of four independent experiments. Table S1. Names of investigated genes. “
“Type 1 diabetes results from a T cell-mediated destruction of insulin-producing pancreatic β cells. Little is known on local factors contributing to migration of T cells to pancreatic tissue. We recently demonstrated evidence of viral infection in β cells in several recent-onset type 1 diabetes patients. Islet inflammation was analysed in a series of new- or recent-onset type 1 diabetic patients and non-diabetic control subjects. Autoimmune T cell reactivity was studied in lymphocytes derived from pancreas-draining lymph nodes of one recent-onset type 1 diabetes patient in partial clinical remission. Insulitic lesions were characterized Suplatast tosilate by presence of β cells, elevated levels

of the chemokine CXCL10 and infiltration of lymphocytes expressing the corresponding chemokine receptor CXCR3 in all pancreatic lesions of type 1 diabetes patients, regardless of enterovirus infection of β cells. CXCR3 and CXCL10 were undetectable in pancreata of non-diabetic control subjects. T cells isolated from draining lymph nodes of a recent-onset patient with virally infected β cells and in clinical remission reacted with multiple islet autoantigens and displayed a mixed interferon (IFN)-γ/interleukin (IL)-10 cytokine pattern. Our data point to CXCL10 as an important cytokine in distressed islets that may contribute to inflammation leading to insulitis and β cell destruction, regardless of local viral infection. We demonstrate further pro- and anti-inflammatory islet autoreactivity, indicating that different adaptive and innate immune responses may contribute to insulitis and β cell destruction.

Thus, the administration of CD40L may not be as useful as that of RANKL for enhancing the self-tolerance-inducing capability of the thymic medulla. It should be also noted that an excess of sRANKL causes osteoporosis by accelerating osteoclastogenesis 49. Thus, the combined application of bisphosphonate may be useful for the prevention of bone resorption caused by sRANKL administration. An improved understanding of the contribution of TNFSF cytokines to thymic medulla formation should offer further clues for the manipulation of

self-tolerance and the development of therapeutic strategies for autoimmune diseases. This study was supported by an MEXT Grant-in-Aid for Scientific Research on Priority Area “Immunological Self. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“Merck

Serono selleck International S. A.– Geneva, Geneva, Switzerland Department of Neurology, University of Magdeburg, Magdeburg, Germany Migration of immune cells characterizes inflammation and plays a key role in autoimmune diseases such as MS. CD4+Foxp3+ regulatory T cells (Treg) have the potential to dampen immune responses but Selisistat purchase show functional impairment in patients with MS. We here show that murine Treg exhibit higher constitutive cell motility in horizontal migration on laminin, surpass non-Treg in transwell assays through microporous membranes as well as across primary brain endothelium and are present in the naïve CNS to a significantly higher extent compared to spleen, lymph nodes and blood. Likewise, human Treg from

healthy donors significantly exceed non-Treg in migratory rates across primary human brain endothelium. Finally, we investigated whether the propensity to migrate is impaired as a feature of autoimmunity and therefore tested patients with MS. Treg from patients with stable relapsing-remitting MS show significantly impaired migratory capacity under non-inflammatory conditions compared to healthy donors. We hypothesize that the enhanced propensity to migrate is a feature of Treg that allows for an equilibrium in parenchymal immune surveillance, e.g. of the CNS. Impaired Treg migration across Epothilone B (EPO906, Patupilone) the intact blood–brain barrier, as observed for Treg from patients with MS, indicates a broader functional deficiency hypothetically contributing to early CNS lesion development or phases of MS remissions. Naturally occurring CD4+Foxp3+ regulatory T cells (Treg) are essential mediators of peripheral immune tolerance, regulating inflammation in the context of infection, autoimmunity, neoplasia and transplant rejection 1. In addition to balancing immunity within lymphoid tissues, Treg enter non-lymphoid target sites of inflammation, exerting their anti-inflammatory function there 2–5. First, regulatory as well as effector T-cell subsets have to undergo a non-lymphoid homing receptor switch after entering secondary lymphoid tissue 6.

, 1998). Here, we tested how different routes of immunization can be used to generate immune responses inducing a protection against CDI, with Cwp84 as an antigen. Immunizations by the intragastric route did not induce an increase of seric Cwp84-specific antibody levels and this result was correlated with the very low animal protection from CDI observed. Antigen degradation by gastric

and intestinal secretions, dilution in the intestinal fluids, poor sampling via Peyer’s patches, may all be factors that contribute to the limited efficiency of the oral route. It seems evident that this route requires that antigens AZD8055 must be protected from degradation by digestive enzymes. The subcutaneous route was the best to induce a high systemic immune response with antibody titres more than twofold higher than that for the intrarectal route. However, in this study, serum Cwp84 antibody titres did not correlate with protection. The best animal protection was observed with the rectal route of immunization. Further studies are needed to specify the immune effectors induced by rectal immunization. Unfortunately, secondary antibodies directed to hamster IgA are not commercially available. This is why we were not able to determine more precisely the specific immune response at the intestinal level. We failed to find evidence of significant neutralization activity against the Cwp84 protease activity in the serum of hamster vaccinated with a protective intrarectal formula

vaccine. These results indicate Cytidine deaminase www.selleckchem.com/products/BIBW2992.html that, in this model, protection is probably not only related to neutralizing antibodies and other factors may play an important role in the host immune response against CDI. Because survival correlated poorly with antibodies titres, it is possible that our immunization strategy generated a wider cell-based immunity that induces partial protection. Recent

data on Streptococcus pneumoniae have demonstrated that multiple immune cell types are required for the induction of a protective immunity in a murine model that lacks mature B cells and fails to produce antibody (Mizrachi-Nebenzahl et al., 2003; McCool & Weiser, 2004). Recently, surface proteins such as the SLPs, because they cover the cell almost completely, have been tested in a series of immunizations combined with different systemic and mucosal adjuvants and challenge experiments in Golden Syrian hamsters (Ni Eidhin et al., 2008). None of the immunization regimens conferred complete protection in the hamster model, and antibody stimulation was variable within regimens, and generally modest. Others have demonstrated the benefits of using a protease as components of vaccines against S. pneumoniae for example. Mucosal immunization with caseinolytic protease (ClpP) antigen induced both systemic and mucosal antibodies, and in this way, reduced lung colonization and also protected mice against death. ClpP has been found to be highly immunogenic and conserved among different strains of S.

TNF polymorphism rs1800630 A-allele was associated with lower specific anti-pneumococcal IgG levels compared with children carrying C/C genotype of rs1800630. Typhoid fever.  Typhoid fever is caused by Salmonella enterica infection with serotype Typhi and 22 million cases of typhoid fever occur worldwide per year, resulting in 200,000 deaths. Indonesian study suggested a protective role of DRB1*12021 for complicated typhoid fever. Keuter et al. [43] found Selleck R788 a lower level of TNF-α in the patients with acute phase of typhoid fever than in convalescence. The seven polymorphisms have been found within the genes BAT1 (a member of the DEAD-box

protein family encoding an ATP-dependent RNA helicase and a negative regulator of inflammation), LTA and TNF. All three genes, or haplotypes spanning these genes, have been associated with a variety of infectious and inflammatory diseases. Dunstan et al. [44] genotyped eighty SNPs in a region of 150 kb in Vietnamese individuals.

Thirty-three SNPs with a minor allele frequency of greater than 4.3% were used to construct haplotypes. Fifteen SNPs which tagged the 42 constructed haplotypes were selected. The haplotype-tagging SNPs (T1–T15) were genotyped, and allelic frequencies of seven SNPs (T1, T2, T3, T5, T6, T7 and T8) have shown a significant difference between typhoid cases and controls. Haplotype-based analysis of the tag SNPs provided positive evidence of association learn more with typhoid. The analysis detected a low-risk cluster of haplotypes that each carries the minor allele of T1 or T7, but not both, and otherwise carries the combination of alleles *12122*1111 at T1–T11. Individuals who carry the typhoid fever–protective haplotype *12122*1111 also produce a relatively low TNF-α response to LPS. Severe sepsis in trauma patients.  In the non-coronary intensive care unit, sepsis is the prevalent cause of death. A restriction fragment length polymorphism (RFLP) present in TNF gene is correlated

with increased level of TNF-α in plasma and a high mortality rate in patients with severe sepsis. This non-synonimous polymorphism in the first intron of the TNF-β gene (1064–1069 position) is responsible PIK3C2G for an amino acid change at position 26 (asparagine for the TNFB1 sequence and threonine for the TNFB2 sequence) [45]. Previously, the mortality rate in severe sepsis was found to be significantly increased in patients homozygous for the allele TNFB2 of the Nco1 polymorphism compared with heterozygous patients [46]. A statistically highly significant association was obtained between the genotype of the biallelic Nco1 polymorphism of the TNF β gene and the development of severe sepsis after severe blunt trauma. Subjects homozygous for the allele TNFB2 have a significantly increased risk of the development of severe post-traumatic sepsis.

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’ PF-01367338 solubility dmso 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 KU-57788 target antigens and can therefore be considered to be a more second 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).

“
“Citation Tang Z, Tadesse S, Norwitz E, Mor G, Abrahams VM., selleck compound Guller S. Isolation of Hofbauer cells from human term placentas with high yield and purity. Am J Reprod Immunol 2011; 66: 336–348 Problem  Placental villus macrophages (i.e., Hofbauer cells, HBCs)

were identified more than 100 years ago. Alterations in their numbers and characteristics are associated with several complications of pregnancy. Although HBCs have previously been isolated and cultured, there is no consensus methodology to obtain these cells with high yield and purity for in vitro studies. Method of study  Hofbauer cells were isolated from human term placentas using protocols in which cytotrophoblasts (CTs) and fibroblasts (FIBs), other major villous cell types, were isolated in parallel. Enzymatic digestion, Percoll gradients, and immunoselection were used to isolate the three cell types. Purity was assessed by morphology, flow cytometry, and phagocytosis

assays. Results  Hofbauer cells were isolated with 98–99% purity and a yield of 130–200 × 106 cells/80–100 g of tissue. HBCs exhibited a pleiomorphic and vacuolated appearance for at least 5 days in culture medium with and without serum. High levels of phagocytosis in HBCs, but not Selleck Wnt inhibitor in CTs or FIBs, confirmed macrophage function in HBCs. Phagocytotic activity was maintained across several days in culture. Conclusion  Hofbauer cells were isolated from term placenta with high yield and purity using protocols in which CTs and FIBs were also obtained. This methodology will foster future

studies that examine the role of HBCs in regulating villus function. “
“The commensal microbiota, most of which resides in the gut, is an environmental regulator of mucosal and systemic immune maturation. Epidemiological studies suggest that changes in the microbiota may represent a link between a modern lifestyle and risk of certain immuno-allergic diseases. This suggests that the microbiota is an appropriate target for therapy or prophylaxis, the rationale for which is addressed here using inflammatory bowel disease as an example. Erastin molecular weight It is also evident from comparative studies of germ-free and conventionally colonized animals that the microbiota is a source of regulatory signals for full development of the host. In some instances these signals have been defined molecularly, and may be suitable for exploitation in novel drug discovery. Most of the versatile drugs in common usage today were derived originally from living matter in the wider environment; could it be time to mine new drugs from microbial-derived signalling molecules in the inner environment of the gut? Several examples illustrate the potential of the gut microbiota as a rich repository from which bioactives with immunological impact can be mined, and translated to human health care or to animal husbandry.

Preceding the initiation codon, a 5′-untranslated region (5′-UTR) of 740 nt is present. The first 100 nt are complementary to the sequence responsible for the initiation of transcription. The subsequent region (100–740 nt) carries the internal ribosomal entry site. The 3′-end of the genome consists of a short UTR of about 70 nt, carrying part of the encapsidation signal followed by a poly (A) sequence

(Westrop et al., 1989). Two vaccines are used for the this website prevention of acute paralytic poliomyelitis: the inactivated poliovirus vaccine of enhanced potency (eIPV) and oral poliovirus vaccine (OPV), composed of three live attenuated virus strains (Sabin et al., 1960; Salk, 1977; Schwartz Ferroptosis inhibitor et al., 1989). OPV is preferred for poliovirus eradication because it multiplies actively in the gut of vaccinees, eliciting

a strong, long-lasting immune response and is less expensive than inactivated poliovirus vaccines. Local immunity induced by OPV prevents or limits reinfection of humans, thereby also preventing natural poliovirus circulation. These properties have made OPV the main vehicle for poliomyelitis eradication (Chumakov, 1961; Schwartz et al., 1989; Strebel et al., 1992; Ghendon & Robertson, 1994; Sutter et al., 2000). However, the vaccines manufactured from the inactivated viruses play a very important role during the ‘endgame’ of CYTH4 the eradication process (Stanway et al., 1983; Kew et al., 2005, 2006). Sabin’s poliovirus strains have generally had good safety records. However, the selection of variants with increased neurovirulence, caused by genetic instability, constituted a real problem with respect to vaccine safety (Anonymous, 1969, 1976; Almond et al., 2007). In early periods of OPV research, such changes were detected by alterations of genetic markers, such as thermosensitivity of reproduction (rct−40 marker), sensitivity of plaque formation to sulfated polysaccharides (d marker)

as well as antigenic modifications (Melnick et al., 1972; Agol, 2006). Vaccine-associated paralytic poliomyelitis (VAPP) has been identified in the case of all three serotypes of the Sabin strains, but the risk proved to be the highest in the case of type 3 (Dömök, 1971, 1984; Furione et al., 1993; Karakasiliotis et al., 2004). In connection with the Global Eradication Program of the wild polioviruses led by WHO, the concept of vaccine-derived poliovirus (VDPV) had to be defined. Long-term excretors were identified whose Sabin-like viruses mutated serially with time. The common antigenic changes in evolving OPV strains were acquired either during the original selection of the vaccine or had been present already in the parental strains (Otelea et al., 1993; Macadam et al., 2006).

Hooibrink, T. van Capel, F. van Alphen, and E. Mul for help with FACS sorting, E.Mul and T. Poplonski for help with ImageStream analysis, and the volunteers for donating blood. We also thank Dr. M. Nolte for critical reading of the manuscript. This work has been supported by the Dutch Science Foundation (VENI 916.76.127, M.C.W.). J.J.K. is supported through a personal VIDI grant (917.66.310; Dutch Science Foundation) to B.B. The authors declare no financial or commercial conflict of interest. Disclaimer: Supplementary materials have been peer-reviewed but not copyedited. Supporting Information Figure 1. (A) NAB2 is induced in human pDCs upon CpG, but not upon type I IFN stimulation.

Primary human pDCs were activated for 4h with 12.5 μg/ml CpG A or 200 ng/ml IFNα, and NAB2 protein levels were assessed. (B-F) CpG activated CAL-1 cells express CD40, IFNβ and MXA, and kill target cells in a TRAIL-dependent manner. CAL-1 GSK3 inhibitor ABT-199 clinical trial cells were left untreated (-) or activated with Control CpG (Ctrl), CpG or IFNβ for 4h, and CD40 protein levels were measured by flow cytometry and compared with isotype control staining of CpG treated CAL-1 cells (B). mRNA levels of CD40 (C), IFNβ (D) and MXA (E) were assessed by RT-PCR. (F) CAL-1-EV cells were left untreated or CpG-activated for 6h prior to co-culture with DDAO-labeled Jurkat cells for 20h in a ratio 25:1. TRAIL-dependent killing was assessed

by adding 10 μg/ml anti-TRAIL antibody to CAL-1 cells 30 min prior to the co-culture (CpG+αTRAIL). Apoptosis induction of DDAO+ Jurkat cells was assessed by AnnexinV or Active Oxymatrine Caspase-3 stainings. Numbers represent the percentage of AnnexinV or Active Caspase-3 positive cells. Data are representative of at least 8 (B-D) or 2 (E-F) independent experiments (**p<0.005, ***p<0.001). Supporting Information Figure 2. Activation of CAL1 cell variants with CpG results

in comparable induction of CD40, TNF-α and IRF-7. CAL-1 cell variants were left untreated (Ctrl) or activated for 6h with CpG. (A) CD40 levels were assessed by flow cytometry. Left panel: one representative analysis of CD40 expression of one of 3 independently performed experiments combined in the right panel. (B) TNF-α and IL-6 cytokine expression were measured in the supernatant of 6h untreated or CpG-stimulated CAL-1 cell variants. (C) IRF-7 expression was measured by intracellular flow cytometry staining in CAL-1-EV, – NAB2, -NAB2E51K untreated or stimulated for o/n with CpG. The mean of GeoMFI of IRF-7 minus isotype control are shown. Data are representative of 3 independent experiments (*p<0.05, ***p<0.001). ND: not detectable. Supporting Information Figure 2. IRF-7 nuclear translocation in CAL-1 cells is not affected by exogenous expression of NAB2 or NAB2E51K. (D-F) CAL-2-EV, -NAB2, or -NAB2E51K were left untreated (Ctrl) or stimulated with CpG for 6h, and IRF-7 translocation was measured with ImageStream technology.

The same UVB treatment protocol was used for all patients based on skin type, with initial doses of 130–400 mJ/cm² with subsequent increases of 15–65 mJ/cm² after each treatment session [15]. Both groups

were advised to use moisturizing creams daily. Patients who received combination treatment and NB-UVB therapy alone were comparable regarding age (mean: 36.7 years [range: 19–57] versus Regorafenib mw 33.7 years [range: 27–42]; P = 0.41), gender (five women/one man and five women/one man) and Psoriasis Area and Severity Index (PASI) [14] (18.2 [range: 7.8–32.2) versus 12.3 [range: 8.2–15.1]; P = 0.19). The only difference was that patients receiving combination treatment had a longer duration of the disease compared with patients receiving NB-UVB therapy (mean:

22.3 years [range: 6–36] versus 12.3 years [range: 5–23]; P = 0.036). VX-809 ic50 The control group consisted of 3 anonymous healthy blood donors from the Landspitali University Hospital (Reykjavik, Iceland) blood bank. Heparinized peripheral venous blood was collected at each time point, and peripheral blood mononuclear cells (PBMC) were obtained by gradient centrifugation with Ficoll-Paque PLUS (Healthcare, Uppsala, Sweden), collected at the interface and washed with HBSS medium (Gibco, Carlsbad, CA, USA) prior to staining with such as anti-human CD3, CD4, CLA, CD103 (all from Biolegend, San Diego, CA, USA), CD8, CD45R0, CD54, CCR4 (all from BD Biosciences, San Jose, CA, USA), IL-23R and CCR10 (both from R&D Systems, Abingdon, UK) monoclonal antibodies (mAbs) for T cell analysis and CD14, CD11c, TLR2 (Biolegend) and TLR6 (HyCult Biotechnology, Uden, The Netherlands) mAbs for monocyte analysis. The PBMC (1.0 × 106 cells/ml) were cultured for 16 h in RPMI 1640 medium with penicillin–streptomycin (100 IU/ml and 0.1 mg/ml) (Gibco), in the presence of anti-CD3 (5 μg/ml), anti-CD28 (5.0 μg/ml) mAbs (Biolegend) and brefeldin A (3.0 μg/ml) (eBioscience,

San Diego, CA, USA) at 37 °C. The T cells were first stained for CD4 and CD8, then fixed and permeabilized and stained intracellularly with anti-human OSBPL9 tumour necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-17A (all from Biolegend) and IL-22 (R&D Systems) mAbs. The cells were washed with phosphate-buffered saline (PBS) prior to fluorescence-activated cell sorting (FACS) analysis. Serum samples were collected at each time point and frozen at −70 °C until used. At the end of the study period, the levels of IL-22, IL-17, IL-23, CCL20, IL-1β and TNF-α were determined by enzyme-linked immunosorbent assays (ELISAs), using commercially available kits (R&D Systems), according to the manufacturer’s instructions. A 3-mm punch biopsy was taken from the arm of each patient at every evaluation. The biopsy was taken from the edge of the thickest lesion on the forearm, then fixed in formaldehyde and stained using HE for histologic evaluation.

Methods: We

analyzed Small molecule library research buy the urinary soluble Klotho levels in a cohort of 161 patients with stage 1–5 CKD and assessed the relationships between the urinary Klotho-to-creatinine ratio (Klotho/Cr), proteinuria and the kidney function. The patients were prospectively followed for two years to monitor for doubling of the baseline serum creatinine concentration and the initiation of renal replacement therapy. Results: Median urinary Klotho/Cr level was 0.35 μg/gCr (0.03–1.64) at baseline. The urinary Klotho/Cr level was positively correlated with eGFR and proteinuria and negatively correlated with changes in proteinuria during the follow-up period. The 117 patients followed for two years were categorized into two groups according to the baseline median urinary Klotho value. The 23 patients had progressed to renal end point. Renal survival was significantly lower in the patients with a urinary Klotho/Cr

ratio of ≤0.321 μg/gCr than in those with a urinary Klotho/Cr ratio of >0.321 μg/gCr (p = 0.0398). A Cox regression analysis adjusted Y-27632 cost for age, gender, hypertension, diabetes, dyslipidemia, eGFR, proteinuria, hemoglobin, phosphate, fibroblast growth factor 23 and renin-angiotensin system blockade showed that a urinary Klotho/Cr ratio of >0.321 was significantly associated with a reduced risk for the renal end point. The adjusted odds ratio for a urinary Klotho/Cr ratio of >0.321 was 0.59 (95% confidential interval: 0.35–0.96; p = 0.0334). Conclusion: In this study, lower levels of urinary Klotho were significantly associated with renal outcomes, suggesting that a lower urinary Klotho level can serve as a novel biomarker for CKD progression. SAXENA ANITA, GUPTA oxyclozanide AMIT, SHARMA RAJKUMAR Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow Introduction: Bioelectric impedance analysis (BIA) a simple noninvasive, bedside method for estimation of water

compartments which can be used in clinical settings. Study was undertaken to evaluate applicability of BIA as a screening tool for presence of kidney disease in general population by estimating body water compartments, creatinine clearance and glomerular filtration rate (GFR). Material and Methods: A cross-sectional non-hospital based study on randomly selected 52 subjects from general population. Maltron BIOSCAN analyzer 915/916 was used for evaluating water cpmpartments, creatinine clearance and GFR. Biochemical tests included hemoglobin, blood sugar random, liver function test (Bilirubin, SGPT, SGOT and Alkaline phosphatase), renal function test (serum creatinine and BUN), uric acid and urine microscopy. Blood pressure was checked.Total body water (TBW) derived using BIA was validated against Hume etal’s equations for estimating TBW. Results: Out of 52 subjects 24 (46.