Project description:Anaplasma phagocytophilum infects a wide variety of host species and causes the diseases granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. The objective of this research was to characterize differential gene expression in wild boar naturally infected with A. phagocytophilum by microarray hybridization using the GeneChip® Porcine Genome Array
Project description:Anaplasma phagocytophilum infects a wide variety of host species and causes the diseases granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. The objective of this research was to characterize differential gene expression in wild boar naturally infected with A. phagocytophilum by microarray hybridization using the GeneChip® Porcine Genome Array Differential gene expression in wild boar naturally infected with A. phagocytophilum was chacarterized by microarray hybridization using the GeneChip® Porcine Genome Array and real-time RT-PCR.
Project description:Gene expression profiling of human promyelocytic cells in response to infection with Anaplasma phagocytophilum. Total RNA derived from 3DPI Anaplasma phagocytophilum-infected HL-60 cells was labeled with A647 and total RNA derived from 3DPI Mock-infected HL-60 cells was labeled with A546. For each, 5 µg of total RNA was labeled using Genisphere Array900, Alexa Fluor dyes and SuperscriptII. Slide scanned with ScanArray Express and images processed with GenePix Pro version 4.0. Normalized log ratios VALUES determined using R-project statistical environment (http://www.r-project.org) and Bioconductor (http://www.bioconductor.org) through the GenePix AutoProcessor (GPAP, http://darwin.biochem.okstate.edu/gpap) website (P. Ayoubi, unpublished results). Keywords: time-course
Project description:Ticks are blood feeding arthropod ectoparasites that transmit pathogens, which cause diseases in humans and animals worldwide. In the past ten decades, the continuous human exploitation of environmental resources and the increase in human outdoor activities has promoted contact with arthropod vectors normally present in the wild, resulting in increased transmission of vector-borne pathogens. In addition, vector populations are expanding in response to climate change and human interventions that impact reservoir host movement and human exposure to infected vectors. Among these emerging vector-borne pathogens, Anaplasma phagocytophilum (Rickettsiales: Anaplasmataceae) has become an important tick-borne pathogen in the United States, Europe and Asia, with increasing numbers of infected people and animals every year. Diseases caused by A. phagocytophilum include human granulocytic anaplasmosis (HGA), equine and canine granulocytic anaplasmosis and tick-borne fever (TBF) in ruminants. The natural infection cycle of A. phagocytophilum is dependent upon the presence of infected vertebrate reservoir hosts and Ixodid tick vectors. In the United States and Europe the main vector species are Ixodes scapularis, Ixodes pacificus, and Ixodes ricinus, while a wide range of mammals, lizards, and birds serve as reservoir hosts for various A. phagocytophilum genotypes. A. phagocytophilum initially infects tick midgut cells and then subsequently develops in salivary glands for transmission to susceptible hosts during tick feeding where the pathogen infects granulocytic cells, primarily neutrophils. Anaplasma phagocytophilum develops within membrane-bound inclusions in the host cell cytoplasm. This pathogen has evolved with its tick and vertebrate hosts through dynamic processes involving genetic traits of the pathogen and hosts that collectively mediate pathogen infection, development, persistence, and survival. However, the mechanisms used by A. phagocytophilum for molecular mechanisms involved in tick-pathogen interactions have not been fully characterized. The objective of this study is to characterize the dynamics of the microRNA response in the tick vector Ixodes scapularis in response to A. phagocytophilum infection. To address this objective, the composition of tick microRNAs was characterize using RNA sequencing in I. scapularis tick cells in response to A. phagocytophilum infection. The discovery of these mechanisms provides evidence that a control strategy could be developed targeted at both vertebrate and tick hosts for more complete control of A. phagocytophilum and its associated diseases.
Project description:Gene expression profiling of human promyelocytic cells in response to infection with Anaplasma phagocytophilum. Total RNA derived from 3DPI Anaplasma phagocytophilum-infected HL-60 cells was labeled with A647 and total RNA derived from 3DPI Mock-infected HL-60 cells was labeled with A546. For each, 5 µg of total RNA was labeled using Genisphere Array900, Alexa Fluor dyes and SuperscriptII. Slide scanned with ScanArray Express and images processed with GenePix Pro version 4.0. Normalized log ratios VALUES determined using R-project statistical environment (http://www.r-project.org) and Bioconductor (http://www.bioconductor.org) through the GenePix AutoProcessor (GPAP, http://darwin.biochem.okstate.edu/gpap) website (P. Ayoubi, unpublished results).
Project description:Anaplasma phagocytophilum is the causative agent of tick-borne fever (TBF) in ruminants and human, equine and canine granulocytic anaplasmosis. A. phagocytophilum modifies host gene expression and immune response. The objective of this work was to analyze differential gene expression in A. phagocytophilum-infected sheep using microarray hybridization and real-time RT-PCR in experimentally and naturally infected animals. Keywords: disease state analysis
Project description:Previously, we observed that a tick salivary protein named sialostatin L2 (SL2) mitigates caspase 1-mediated inflammation upon Anaplasma phagocytophilum infection. Here we are performing next-generation sequencing to determine the global effect of SL2 upon A. phagocytophilum infection of macrophages.
Project description:Previously, we observed that a tick salivary protein named sialostatin L2 (SL2) mitigates caspase 1-mediated inflammation upon Anaplasma phagocytophilum infection. Here we are performing next-generation sequencing to determine the global effect of SL2 upon A. phagocytophilum infection of macrophages. BMDMs were treated by 4 different conditions (including non-treated, treated by SL2, treated by Anaplasma, and by Anaplasma and SL2, each treatment was performed in triplicate) followed by the extraction of total RNA and deep sequencing by Illumina