20 research outputs found

    Peniagone-leander New Species, An Abyssal Benthopelagic Sea-Cucumber (Echinodermata, Holothuroidea) From The Eastern Central Pacific-Ocean

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    Peniagone leander. new species, differs from other Peniagone species in possessing the combination of: an ovoid body, lateral ridges defining right and left margins of body, anterior veil (velum) with four projections, two pairs of anterior dorsal projections posterior to velum, four pairs of posterior ventral tube feet. The reddish-brown body reaches a length of approximately 30 em. P. leander is the second species of the genus known to be benthopelagic. The species is fairly common where it occurs, dividing its time between actively swimming above the bottom and feeding on the sediment surface

    Insights into the abundance and diversity of abyssal megafauna in a polymetallic-nodule region in the eastern Clarion-Clipperton Zone

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    There is growing interest in mining polymetallic nodules in the abyssal Clarion-Clipperton Zone (CCZ) in the Pacific. Nonetheless, benthic communities in this region remain poorly known. The ABYSSLINE Project is conducting benthic biological baseline surveys for the UK Seabed Resources Ltd. exploration contract area (UK-1) in the CCZ. Using a Remotely Operated Vehicle, we surveyed megafauna at four sites within a 900 km2 stratum in the UK-1 contract area, and at a site ~250 km east of the UK-1 area, allowing us to make the first estimates of abundance and diversity. We distinguished 170 morphotypes within the UK-1 contract area but species-richness estimators suggest this could be as high as 229. Megafaunal abundance averaged 1.48 ind. m−2. Seven of 12 collected metazoan species were new to science, and four belonged to new genera. Approximately half of the morphotypes occurred only on polymetallic nodules. There were weak, but statistically significant, positive correlations between megafaunal and nodule abundance. Eastern-CCZ megafaunal diversity is high relative to two abyssal datasets from other regions, however comparisons with CCZ and DISCOL datasets are problematic given the lack of standardised methods and taxonomy. We postulate that CCZ megafaunal diversity is driven in part by habitat heterogeneity.This open access work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0

    Transcriptome Analysis Describing New Immunity and Defense Genes in Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis Patients

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    Background: Large-scale gene expression profiling of peripheral blood mononuclear cells from Rheumatoid Arthritis (RA) patients could provide a molecular description that reflects the contribution of diverse cellular responses associated with this disease. The aim of our study was to identify peripheral blood gene expression profiles for RA patients, using Illumina technology, to gain insights into RA molecular mechanisms. Methodology/Principal Findings: The Illumina Human-6v2 Expression BeadChips were used for a complete genome-wide transcript profiling of peripheral blood mononuclear cells (PBMCs) from 18 RA patients and 15 controls. Differential analysis per gene was performed with one-way analysis of variance (ANOVA) and P values were adjusted to control the False Discovery Rate (FDR < 5%). Genes differentially expressed at significant level between patients and controls were analyzed using Gene Ontology (GO) in the PANTHER database to identify biological processes. A differentially expression of 339 Reference Sequence genes (238 down-regulated and 101 up-regulated) between the two groups was observed. We identified a remarkably elevated expression of a spectrum of genes involved in Immunity and Defense in PBMCs of RA patients compared to controls. This result is confirmed by GO analysis, suggesting that these genes could be activated systemically in RA. No significant down-regulated ontology groups were found. Microarray data were validated by real time PCR in a set of nine genes showing a high degree of correlation. Conclusions/Significance: Our study highlighted several new genes that could contribute in the identification of innovative clinical biomarkers for diagnostic procedures and therapeutic interventions

    Host Transcription Factors in the Immediate Pro-Inflammatory Response to the Parasitic Mite Psoroptes ovis

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    BACKGROUND: Sheep scab, caused by infestation with the ectoparasitic mite Psoroptes ovis, results in the rapid development of cutaneous inflammation and leads to the crusted skin lesions characteristic of the disease. We described previously the global host transcriptional response to infestation with P. ovis, elucidating elements of the inflammatory processes which lead to the development of a rapid and profound immune response. However, the mechanisms by which this response is instigated remain unclear. To identify novel methods of intervention a better understanding of the early events involved in triggering the immune response is essential. The objective of this study was to gain a clearer understanding of the mechanisms and signaling pathways involved in the instigation of the immediate pro-inflammatory response. RESULTS: Through a combination of transcription factor binding site enrichment and pathway analysis we identified key roles for a number of transcription factors in the instigation of cutaneous inflammation. In particular, defined roles were elucidated for the transcription factors NF-kB and AP-1 in the orchestration of the early pro-inflammatory response, with these factors being implicated in the activation of a suite of inflammatory mediators. CONCLUSIONS: Interrogation of the host temporal response to P. ovis infestation has enabled the further identification of the mechanisms underlying the development of the immediate host pro-inflammatory response. This response involves key regulatory roles for the transcription factors NF-kB and AP-1. Pathway analysis demonstrated that the activation of these transcription factors may be triggered following a host LPS-type response, potentially involving TLR4-signalling and also lead to the intriguing possibility that this could be triggered by a P. ovis allergen

    Paediatric schistosomiasis:What we know and what we need to know

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    Schistosomiasis affects over 200 million people worldwide, most of whom are children. Research and control strategies directed at preschool-aged children (PSAC), i.e., ≤5 years old, have lagged behind those in older children and adults. With the recent WHO revision of the schistosomiasis treatment guidelines to include PSAC, and the recognition of gaps in our current knowledge on the disease and its treatment in this age group, there is now a concerted effort to address these shortcomings. Global and national schistosome control strategies are yet to include PSAC in treatment schedules. Maximum impact of schistosome treatment programmes will be realised through effective treatment of PSAC. In this review, we (i) discuss the current knowledge on the dynamics and consequences of paediatric schistosomiasis and (ii) identify knowledge and policy gaps relevant to these areas and to the successful control of schistosome infection and disease in this age group. Herein, we highlight risk factors, immune mechanisms, pathology, and optimal timing for screening, diagnosis, and treatment of paediatric schistosomiasis. We also discuss the tools required for treating schistosomiasis in PSAC and strategies for accessing them for treatment

    S100A12 Is Part of the Antimicrobial Network against Mycobacterium leprae in Human Macrophages

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    Submitted by Sandra Infurna ([email protected]) on 2016-12-27T16:28:52Z No. of bitstreams: 1 euzenir_sarno_etal_IOC_2016.pdf: 7892769 bytes, checksum: 863f425230a369832bb3025f695098b9 (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2016-12-27T16:44:36Z (GMT) No. of bitstreams: 1 euzenir_sarno_etal_IOC_2016.pdf: 7892769 bytes, checksum: 863f425230a369832bb3025f695098b9 (MD5)Made available in DSpace on 2016-12-27T16:44:36Z (GMT). No. of bitstreams: 1 euzenir_sarno_etal_IOC_2016.pdf: 7892769 bytes, checksum: 863f425230a369832bb3025f695098b9 (MD5) Previous issue date: 2016University of California. Department of Microbiology, Immunology and Molecular Genetics,. Los Angeles, CA, USA.David Geffen School of Medicine at University of California. Division of Dermatology, Los Angeles, CA, USA.University of California. Department of Microbiology, Immunology and Molecular Genetics,. Los Angeles, CA, USA.University of California. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.David Geffen School of Medicine at University of California. Division of Dermatology, Los Angeles, CA, USA.David Geffen School of Medicine at University of California. UCLA/Orthopedic Hospital Department of Orthopedic Surgery. Los Angeles, CA, USA.David Geffen School of Medicine at University of California. Division of Dermatology, Los Angeles, CA, USA.University of California. Department of Bioengineering. Los Alngeles, CA, USA.University of California. Department of Bioengineering. Los Alngeles, CA, USA.University of California. Department of Bioengineering. Los Alngeles, CA, USA.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ. Brasil.University of Southern California School of Medicine. Department of Dermatology. Los Angeles, CA, USA.University of Southern California School of Medicine. Department of Dermatology. Los Angeles, CA, USA.University of California. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.University of California. Department of Microbiology, Immunology and Molecular Genetics,. Los Angeles, CA, USA / David Geffen School of Medicine at University of California. Division of Dermatology, Los Angeles, CA, USA.Triggering antimicrobial mechanisms in macrophages infected with intracellular pathogens, such as mycobacteria, is critical to host defense against the infection. To uncover the unique and shared antimicrobial networks induced by the innate and adaptive immune systems, gene expression profiles generated by RNA sequencing (RNAseq) from human monocyte-derived macrophages (MDMs) activated with TLR2/1 ligand (TLR2/1L) or IFN-γ were analyzed. Weighed gene correlation network analysis identified modules of genes strongly correlated with TLR2/1L or IFN-γ that were linked by the "defense response" gene ontology term. The common TLR2/1L and IFN-γ inducible human macrophage host defense network contained 16 antimicrobial response genes, including S100A12, which was one of the most highly induced genes by TLR2/1L. There is limited information on the role of S100A12 in infectious disease, leading us to test the hypothesis that S100A12 contributes to host defense against mycobacterial infection in humans. We show that S100A12 is sufficient to directly kill Mycobacterium tuberculosis and Mycobacterium leprae. We also demonstrate that S100A12 is required for TLR2/1L and IFN-γ induced antimicrobial activity against M. leprae in infected macrophages. At the site of disease in leprosy, we found that S100A12 was more strongly expressed in skin lesions from tuberculoid leprosy (T-lep), the self-limiting form of the disease, compared to lepromatous leprosy (L-lep), the progressive form of the disease. These data suggest that S100A12 is part of an innate and adaptive inducible antimicrobial network that contributes to host defense against mycobacteria in infected macrophages

    Vesicular Location and Transport of S100A8 and S100A9 Proteins in Monocytoid Cells.

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    We show here, by using surface biotinylation, followed by Western blotting or surface plasmon resonance analysis, that very low levels of S100A8 and/or S100A9 can be detected on the surface of THP-1 cells or freshly isolated human monocytes. This was supported by immune-electron microscopy where we observed membrane-associated expression of the proteins restricted to small patches. By using confocal microscopy we could determine that S100A8 and S100A9 protein in THP-1 cells or freshly isolated human monocytes was mostly present in vesicular structures. This finding was confirmed using immune-electron microscopy. Subcellular fractionation and confocal microscopy showed that these vesicular structures are mainly early endosomes and endolysosomes. Our subsequent studies showed that accumulation of S100A8 and S100A9 in the endolysosomal compartment is associated with induction of their release from the cells. Furthermore, an inhibitor of lysosomal activity could modulate the release of S100A8 and S100A9 in the extracellular milieu. Our current results suggest that the S100A8 and S100A9 proteins are primarily associated with certain kinds of cytosolic vesicles and may be secreted via an endolysosomal pathway
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