5) Taken together, these

5). Taken together, these HM781-36B data suggest that astrocytes might be able to develop into antigen-presenting cells during the late phase of EAE, thereby contributing to lymphocyte-mediated disease pathogenesis and resulting in severe presentation

of disease. CNS factors have been shown to contribute equally (with immune cells) to MS disease progression [4]. Data presented in this report demonstrate that astrocytes act both as suppressors and promoters of MOG35–55-specific lymphocyte responses; these are associated closely with the disease stage and the local microenvironment. Therefore, targeting of astrocytes during the optimal time-points in the course of disease progression may be used to develop novel EAE therapeutic strategies. This research was supported by the Master Innovation Research Foundation of Hei Longjiang Province (YJSCX2011-325HLJ), the Natural Science Foundation for Youth of China (30901330; 81000512; 81100883), the Natural Science Foundation of China (81171121), the Doctoral Fund of the Ministry of Education of China (20102307110013) and Open project of key laboratory of Myocardical Ischemia Mechanism and Treatment (KF201013). The authors have declared that no competing

interests exist. “
“Acute graft versus host disease (aGVHD) remains a life-threatening complication of bone marrow transplantation. Here we show that IL-27, a member of the IL-12 cytokine family, plays an essential role in a parent-to-F1 murine aGVHD model, using B6 mice as parents and B6D2 mice as F1 recipients. IL-27 is transiently detectable PF-02341066 manufacturer in the serum

of B6D2 recipients of B6 spleen cells, with a peak at day 10. Treatment with anti-IL-27p28 mAb MM27.7B1 (αp28Ab), at the time of and six days after B6 cell transfer, Adenosine triphosphate blocked GVHD. Protection was associated with host cell survival and undiminished engraftment of donor cells, lack of host B-cell depletion, increased Th2-type immunoglobulin production, a decrease in serum IFN-γ, a drop in anti-H-2Dd cytotoxic T lymphocyte activity and an increase in Foxp3+ T cells. We therefore conclude that IL-27 plays a critical role in the parent-to-F1 model of aGVHD and that blocking IL-27 could have therapeutic relevance. “
“According to the hygiene hypothesis, the increased incidence of allergic and autoimmune diseases in developed countries is mainly explained by the decreased contact between the human population and certain environmental agents as lactobacillus, mycobacteria and helminths. In this study, we evaluated the effect of multiple infections with Strongyloides venezuelensis on the development of experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Multiple infections before EAE induction were not able to change the evolution of the disease. No alterations were observed in weight loss, clinical score and inflammation intensity at the central nervous system. The presence of significant levels of parasite-specific IgG1 but not IgG2b suggested a Th2 polarization.

The income is generated through the sale of Karunya Lottery which

The income is generated through the sale of Karunya Lottery which is exclusively devoted for extending financial assistance to this purpose. Hence this finance is fully contributed by the public. Kerala government buy Talazoparib started free karunya dialysis scheme 6 months ago which provide 2 hemodialysis per week irrespective of the residual renal function. We conducted a study to compare

the surogate markers of dialysis adequacy between patients undergoing hemodialysis in karunya dialysis scheme and in private sector. Methods: This was a cross-sectional observational study. All the 83 patients who were undergoing Hemodialysis under karunya scheme in our institution (Government medical college kerala,

India) and 100 patients undergoing hemodialysis in 3 randomly selected dialysis centers under private sector in our city were enrolled into our study. Patients informations were retrieved from from dialysis unit using a data entry form. The information retrieved included patients demographic data, etiology of ESRD, frequency of hemodialysis, types of vascular access used for hemodialysis, frequency of intravenous iron therapy and ESA and the frequency of blood transfusion. The surrogate markers for adequacy selleck screening library like Hemoglobin, ferritin, Albumin, Calcium, phosphrous PTH, lipid profile, signs of fluid overload, uraemic symptoms and biometrics

like midarm circumference, BMI and triceps skin fold thickness were compared between the 2 groups. We also looked at the quality of life based on WHO-QOL BREF questionaries in both the groups. Statistical analysis was done using SPSS version 4-Aminobutyrate aminotransferase 21.0. Results: There were no statistical difference between the two groups in all the parameters compared. Conclusion: Karunya free Dialysis Scheme is an effective way for improving the access to maintenance hemodialysis and renal care without compromising on the outcome and quality of life. Hence we suggest karunya model of dialysis to all End Stage Renal Disease (ESRD) patients in resouce poor countries. HUNG CHI-CHIH, CHANG JER-MING, TSAI JER-CHIA, CHEN HUNG-CHUN Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University Introduction: Higher hemodialysis (HD) adequacy presented as Kt/V is associated with lower all-cause mortality in observational studies, though randomized HEMO study showed no superior survival of higher target Kt/V group patients (Kt/V 1.65 vs Kt/V 1.25). Some subgroups of HD patients such as Asian people or female may have benefits under higher Kt/V. Thus, we would ask whether higher Kt/V with the dose more than that in HEMO study would be associated better survival after long term follow-up.

To rule out the possible influence of diabetes on our results, we

To rule out the possible influence of diabetes on our results, we have analysed differences in fibrinolysis and coagulation parameters between BP patients and normal controls after the exclusion of the three diabetic BP patients and their R788 mouse sex- and age-matched

controls. In the 17 BP patients with active disease, PAI-1 antigen and active PAI-1 levels were significantly higher (22·13 ± 8·68 ng/ml and 16·76 ± 5·55 ng/ml) than in the 17 sex- and age-matched healthy controls (8·65 ± 6·29 ng/ml and 6·21 ± 4·37 ng/ml) (P = 0·0001 for both). Plasma t-PA levels were also significantly higher in the 17 patients (36·91 ± 32·02 ng/ml versus 6·09 ± 4·45 ng/ml; P = 0·0001). Finally, plasma d-dimer and F1+2 levels were both markedly higher in

the 17 patients with active BP (2774 ± 3817 ng/ml and 631 ± 487 ng/ml) than in the 17 controls (183 ± 107 ng/ml and 106 ± 44 ng/ml) (P = 0·0001 for both). In the patients with active BP, disease severity (expressed as the percentage of involved body surface area) correlated significantly with the number of blood eosinophils (r = 0·705, P = 0·01) and the plasma levels of d-dimer (r = 0·713, P = 0·0001) and F1+2 (r = 0·703, P = 0·001). Plasma CRP levels correlated directly with the levels of PAI-1 antigen (r = 0·722, P = 0·0001), PAI-1 activity (r = 0·514, P = 0·021), t-PA antigen (r = 0·547, P = 0·012) and F1+2 (r = 0·450, P = 0·047) and the number of blood eosinophils PD0325901 research buy correlated with PAI-1 antigen (r = 0·585, P = 0·046), PAI-1 activity (r = 0·680, P = 0·015) and d-dimer (r = 0·710, P = 0·010). Anti-BP180 autoantibody levels only correlated with d-dimer (r = 0·495,

P = 0·026) and F1+2 (r = 0·458, P = 0·042). In the 20 BP patients during remission after treatment, the levels of PAI-1 antigen and active Atazanavir PAI-1 decreased significantly from 25·06 ± 8·88 ng/ml to 16·99 ± 7·05 ng/ml and from 15·65 ± 5·75 ng/ml to 11·19 ± 5·14 ng/ml (P = 0·008 and P = 0·006, respectively) (Fig. 1). The mean differences were 5·30 ng/ml [95% confidence interval (CI): 1·65–8·96 ng/ml] for PAI antigen and 4·00 ng/ml (95% CI: 1·66–6·35 ng/ml) for active PAI. There was an albeit not significant decrease in tPA levels (from 34·70 ± 33·22 to 32·74 ± 27·80 ng/ml). Plasma TAFI levels did not change significantly (Fig. 2), but there was a significant decrease in the plasma levels of d-dimer (from 2350 ± 3676 ng/ml to 571 ± 651; P = 0·0001) and F1+2 (from 551 ± 484 ng/ml to 188 ± 216; P = 0·0001). The mean differences were 2804 ng/ml (95% CI: 744–4865 ng/ml) for d-dimer and 414 ng/ml (95% CI: 191–638 ng/ml) for F1+2.

The appreciation that tissue-derived CD103+ DCs in mice, and BDCA

The appreciation that tissue-derived CD103+ DCs in mice, and BDCA3hi DCs in humans, appear to be functionally

and developmentally very closely related to CD8+ DCs, but do not express CD8, has recently lead to the proposal to define this lineage of DCs by their expression of XCR1 [5, 6], a chemokine receptor that is conserved between the different DC subsets and across the species. In Enzalutamide molecular weight addition to this proposed DC lineage, DCs expressing high levels of surface CD11b appear to be functionally biased toward promoting MHC class II-restricted CD4+ T-cell responses [7]. However, only a proportion of splenic CD11bhi DCs express CD4, and tissue-resident CD11bhi DCs are characterized by CD205 expression rather than CD4 [8]. Consequently, the cohort of CD11bhi DCs appears considerably more heterogeneous compared with the relatively well-defined CD8+/XCR1+ lineage [4, 9]. This view is supported by the diverse range of transcription factors and molecules that have been implicated in the development of CD11bhi DCs [10]. Interestingly, it

was recently shown that differential JQ1 ic50 requirement for Notch 2 receptor signaling defines two distinct lineages within the CD11bhi DC population [11]. The Notch 2 receptor signaling-dependent CD11bhi DC population is characterized by high-level expression of ESAM, an immunoglobulin superfamily molecule previously associated with neutrophil extravasation [12], and ESAMhi CD11bhi DC have been described as potent inducers of CD4+

T-cell priming [11]. Conversely, ESAMlo CD11bhi DCs develop independently Methane monooxygenase of Notch 2 receptor signaling and have a gene expression signature resembling that of monocytes [11]. However, exactly how ESAMhi and ESAMlo CD11bhi DCs diverge during development and what factors control Notch 2 receptor signaling in CD11bhi DCs remains obscure. In this issue of the European Journal of Immunology, Beijer et al. [13] have described an unexpected role for vitamin A in promoting the development of these newly described ESAMhi CD11bhi DCs within the spleen. Vitamin A, or retinol, is acquired through dietary intake and stored predominantly within the liver before release into the circulation. Upon conversion of circulating vitamin A into its active metabolite retinoic acid (RA) by retinaldehyde dehydrogenase (Raldh), RA acts as a transcriptional regulator, binding retinoic acid receptors (RAR), and retinoic X receptors (RXR) that are located in the nucleus. The binding of RA to RAR/RXR heterodimers facilitates the recruitment of coactivators and the formation of transcriptional complexes that dock onto RA response elements within the regulatory regions of target genes, which in turn initiates transcription [14]. Vitamin A has long been appreciated for its essential role in host immunity, and more recently has gained considerable attention as a major player in controlling intestinal immunity [15].

Pre- and post-immunization sera prior to challenge (BC) were coll

Pre- and post-immunization sera prior to challenge (BC) were collected on days 0 and 44 by tail bleeding. Prior to euthanasia, post-challenge blood (PC) was drawn from the heart by cardiac puncture. The sera were stored at −20°C CDK inhibitor until further analysis. Brain and lung tissues were obtained under aseptic conditions and were stored at −20°C for subsequent assessment of parasite load by real-time PCR. The spleens were placed into RNA stabilization reagent (Qiagen, Hombrechtikon, Switzerland) and frozen at −80°C for subsequent measurement of cytokines’ expression levels. DNA extraction

from lungs and brain was performed as previously described [28, 29]. The DNA concentrations in all samples were determined by UV spectrophotometry (NanoDrop™, Thermo Scientific, Lausanne, Switzerland) and adjusted to 100 ng/μL with sterile DNase free water. Neospora-specific quantitative real-time PCR was performed using the Rotor-Gene 6000 real-time PCR machine (Corbett Research, Qiagen). The parasite counts were calculated by interpolation from a standard curve with

DNA equivalents from 1000, 100 and buy AZD6738 10 tachyzoites included in each run as previously described [29]. Sera were diluted 1 : 50 and analysed for the presence of antigen-specific IgG, IgG1 and IgG2a by ELISA using purified recNcPDI (400 ng/well) as antigen and anti-mouse IgG alkaline phosphatase conjugate as secondary antibody (1 : 1000; Promega, Madison, WI, USA) or goat anti-mouse alkaline phosphatase IgG1 or IgG2a conjugates (1 : 2000; SouthernBiotech, Birmingham, AL, USA) [28, 29]. Absorbance values (405 nm) were read in a microplate reader (Dynatech, Embrach, Switzerland). Spleens were harvested at the time of death or latest at 40 days post-challenge and were processed for RNA isolation as Niclosamide previously described [18]. First-strand cDNA synthesis was performed using the Omniscript® Reverse Transcription kit (Qiagen) in a final volume of 20 μL containing 1 μg

of total RNA and 0·5 μg random primers (Promega,Walisellen, Switzerland). DNA fragments of mouse β-actin and of four different cytokines (IL-4, IL-10, IL-12 and IFN-γ) were amplified from each cDNA using the QuantiTec™SYBR® Green PCR kit (Qiagen) and previously designed primer pairs [30]. To quantify IL-17A and Foxp3 transcript levels, forward primers IL-17A-f (5′-TCTCTGATGCTGTTGCTGCT-3′) and reverse primers IL-17A-r (5′-CGTGGAACGGTTGAGGTAGT-3′) or forward Foxp3-f (5′-GAGAAAGCGGATACCAAA-3′) and reverse primers Foxp3-r (5′-TGTGAGGACTACCGAGCC-3′) were used. The quantitative PCR was performed on a Rotor-Gene 6000 real-time PCR machine (Corbett Research, Qiagen) as previously described [18]. Fluorescence was measured after each cycle at 80°C. To calculate the slope and the efficiency of the PCR, serial 10-fold dilutions of probes were included for each primer pair, and a standard curve was generated.

3,[73] which has been reported to destabilize nucleosomes [74] A

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 PCI-32765 solubility dmso 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 Fostamatinib 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 Sinomenine 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.

In retrospect, what I found of interest was the

In retrospect, what I found of interest was the see more reaction of myself and my colleagues to this incident. Our department consists of no less than than seven labs working on Plasmodium: molecular biologists, immunologists and protein biochemists working both in vivo and in vitro, on both human and rodent strains. Yet the guy became the talking point for the whole day. Despite daily contact with the parasite at the bench, in the culture hood or in the insectary, none of us were quite prepared for being confronted by the parasite in the most natural and pertinent of settings: a sick man. Monday

April 25th is World Malaria Day 2011. http://www.rbm.who.int/worldmalariaday/ Matthew Lewis Parasitology Department, University of Heidelberg, Germany. E-mail: [email protected]
“Cytotoxic T lymphocytes (CTLs) kill tumorigenic and virally infected cells by targeted secretion of lytic granule contents. The precise point at which secretion occurs

is directed by the centrosome docking at the immunological synapse (IS). The centrosome is highly dynamic in CTLs, lagging behind the nucleus in the uropod of migrating CTLs, but translocating Dasatinib chemical structure across the entire length of the cell to dock at the IS when a target cell is recognized. While in most cell types, the centrosome is always closely associated with the nuclear membrane, in CTLs, it often appears to be dissociated from the nucleus, both in migrating cells and when forming an IS. We asked

whether this dissociation is required for CTL killing, by expressing GFP-BICD2-NT-nesprin-3, which tethers the centrosome to the nucleus irreversibly. Immunofluorescence microscopy revealed that the Casein kinase 1 centrosome polarized successfully to the central supramolecular activation complex (cSMAC) of the synapse in GFP-BICD2-NT-nesprin-3-expressing CTLs, with the centrosome and nucleus migrating together to the IS. CTLs in which the centrosome was “glued” to the nucleus were able to dock and release granules at the IS as effectively as mock-treated cells. These data demonstrate that CTL cytotoxicity is independent of centrosomal dissociation from the nuclear envelope. “
“Vaccination with the non-adjuvanted split-virion A/California/7/2009 influenza vaccine (pandemic H1N1 2009 vaccine) began in October 2009 in Japan. The present study was designed to assess the effect of prior vaccination with a seasonal trivalent influenza vaccine on the antibody response to the pandemic H1N1 2009 vaccine in healthy adult volunteers. One hundred and seventeen participants aged 22 to 62 were randomly assigned to two study groups.

Controls were 115 voluntary healthy bone marrow donors recruited

Controls were 115 voluntary healthy bone marrow donors recruited at the blood bank of the Service of Immunology at the Hospital de Clínicas de Porto Alegre, most of them resident in the urban area of Porto Alegre/RS (83 women and 32 men; 86·1% European descendents and 13·9% African descendents). Individuals presenting chronic or acute diseases were excluded from the sample, as well as those presenting family history of genetic diseases (X-linked, autosomal or chromosomal abnormalities). this website Amerindians and subjects

with Asiatic origin were not included. All patients were interviewed and examined according to an extensive questionnaire directed to the evaluation of end-organ damage [14]. Disease subtype was classified as follows: diffuse cutaneous SSc (truncal and acral skin tautness), limited cutaneous SSc (skin tautness restricted to extremities

and/or face) and limited SSc (sine scleroderma) [13,15]. Clinical characteristics of the disease were observed and recorded as described previously [14]. Blood samples were collected for serology [anti-nuclear antibodies (ANA), anti-centromere and anti-topoisomerase I antibodies] and DNA extraction. Pulmonary high-resolution computed tomography (HRCT) was performed in most patients. Doppler echocardiography was used to estimate the pulmonary systolic arterial pressure (PSAP), and patients with PSAP ≥ 40 mmHg were considered to have pulmonary arterial hypertension. This study was approved by the Research Ethics Board of Hospital de Clínicas de Porto Alegre (IRB0000921). Selleck CT99021 Phosphatidylinositol diacylglycerol-lyase All patients and controls signed a written informed consent before participating in this study. DNA was extracted from blood buffy coat using a modified salting-out technique, as described by Miller SA et al.[16]. Fifteen KIR genes (2DS1, 2DS2, 2DS3, 2DS4, 2DS5, 3DS1, 2DL1, 2DL2,

2DL3, 2DL4, 2DL5, 3DL1, 3DL2, 3DL3 and 2DP1) were typed in patients and controls using a polymerase chain reaction with sequence specific primers (PCR–SSP) method, as described by Gomez-Lozano et al.[17]. For the PCR, 10 ng DNA, 50 mM MgCl2, 1 µl PCR buffer, 25 mM deoxyribonucleoside triphosphates (dNTPs), 500 nM primers, 100 nm internal control and 2·5 units of Taq polymerase were mixed in a total volume of 10 µl [internal control primers amplify a 796 base pairs (bp) fragment of the third intron of human leucocyte antigen (HLA) DRB1]. PCR products were amplified by the GeneAmp PCR system 9600 (Perkin-Elmer, Norwalk, CA, USA), with denaturation for 3 min at 94°C, followed by four cycles of 15 s at 94°C, 15 s at 65°C, 15 s at 72°C; 21 cycles of 15 s at 94°C, 15 s at 60°C, 30 s at 72°C; five cycles of 15 s at 94°C, 1 min at 55°C, 2 min at 72°C; and a final elongation step at 72°C for 7 min. The PCR products were analysed on 1% agarose gel after electrophoresis.

, 1997; Casjens et al , 2000) Although the B  burgdorferi chromo

, 1997; Casjens et al., 2000). Although the B. burgdorferi chromosome is rather small (approximately one megabase), the complexity and large sizes of many of the plasmids (some larger than 50 kb) greatly expand the DNA coding capacity of this spirochete. At the same time, however, it is currently poorly understood what role surface proteins encoded by genes on the various plasmids contribute to virulence and/or disease pathogenesis. The data accumulated thus far overwhelmingly support the hypothesis that plasmid-encoded proteins

are important in Lyme disease pathogenesis Talazoparib in vitro and could encode antigens that are important virulence factors and/or potential vaccinogens for Lyme disease. Given that the first vaccine developed for Lyme disease was generated against the fairly well conserved, plasmid-encoded OspA, it seems likely that HKI 272 the identification of another outer surface protein that is well conserved throughout borrelial genospecies would be a viable candidate for a developing a new vaccine molecule. This review outlines the outer surface proteins that have been identified thus far in various borrelial species, although the main focus is on the type

strain B. burgdorferi strain B31. The outer surface proteins described below fall into two main categories, lipid-modified outer surface proteins that are anchored to the outer leaflet of the outer membrane through their lipid moieties (e.g. OspA, OspB, OspC, OspD, OspE, OspF, DbpA, DbpB, CspA, VlsE, BptA, and several others with no known function) and outer surface proteins that have one or more transmembrane domains that anchor them into the outer membrane (e.g. P13, P66, BesC, BamA, Lmp1, and BB0405). The sections following provide a detailed examination of what is currently known about outer surface lipoproteins and membrane-spanning OMPs of B. burgdorferi. The B. burgdorferi genome Amylase encodes several lipoproteins that are localized to the surface of B. burgdorferi (Fraser et al., 1997; Casjens

et al., 2000). The surface lipoproteins of B. burgdorferi are now well recognized as important virulence determinants. As mentioned previously, because of the extracellular nature of this pathogen, surface lipoproteins play an important role in virulence, host–pathogen interactions, and in maintaining the enzootic cycle of B. burgdorferi. Several borrelial surface lipoproteins have been identified that bind host proteins and promote the adherence to host cells. For instance, B. burgdorferi lipoproteins bind host glycosaminoglycans (GAGs), decorin, and fibronectin. Furthermore, lipoproteins have been implicated in evasion of the host immune response through antigenic variation and evasion of complement deposition.

CFDA and propidium iodide fluorescence were detected by flow cyto

CFDA and propidium iodide fluorescence were detected by flow cytometry. Proliferation was calculated by relating the mean fluorescence intensity to cells grown in IL-2 alone (100 % proliferation) and cells cultured in the presence of the mitosis inhibitor Colcemide (50 ng/mL, Biochrom) (0 % proliferation). This study was supported by grant HA 4318/37hyphen;3

from Deutsche Forschungsgemeinschaft (DFG). 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 see more available as submitted by the authors. “
“The prevalence of OXA-type carbapenemase genes, ISAba1 insertion sequence, carbapenem resistance, biofilm forming ability and genetic heterogeneity in clinical isolates of Acinetobacter spp. from hospitals in Mangalore, South India was studied. Based on the presence of the blaOXA-51-like gene, the 62 isolates of Acinetobacter spp. were identified as 48 A. baumannii and 14 other Acinetobacter spp. The prevalence of blaOXA-23-like, blaOXA-24-like and blaOXA-58-like

genes in A. baumannii was 47.9%, 22.9% and 4.2%, while in other Acinetobacter spp. it was 28.5%, 64.3% and 35.7% respectively. Several A. baumannii isolates (16/48) harbored the insertion sequence ISAba1 in the upstream region of the blaOXA-23-like Wnt inhibitor gene. Resistance to meropenem was seen in 39.6% and 14.2% of A. baumannii and other Acinetobacter spp. isolates, respectively. The ability to form biofilm was observed to be higher among A. baumannii in comparison to other Acinetobacter spp. The present study shows that blaOXA-23-like

Org 27569 genes are more common in A. baumannii,whereas blaOXA-24-like genes are common to other Acinetobacter spp. The study revealed genetic heterogeneity among the isolates, indicating multiple sources in the hospitals. Acinetobacter spp., particularly, Acinetobacter baumannii have emerged as an important nosocomial pathogen worldwide (1), multiple drug resistance posing a serious problem in the clinical management of infections caused by them. Surveys by the British Society for Antimicrobial Chemotherapy in 2005 showed that >30% of bacteremia isolates were resistant to gentamicin and other drugs, resistance to imipenem being low (2). Carbapenem resistance mechanisms are mediated by beta-lactamases which are classified by two general schemes: the Ambler molecular scheme and the Bush-Jacoby-Medieros scheme (3, 4). In the Ambler molecular scheme, beta-lactamases are classified into four major types, A – D, based on protein homology. This excludes the phenotypic basis that is commonly used in any laboratory. Classes A, C and D are serine-beta-lactamases while class B includes metallo-beta-lactamases.