E-GEOD-87643
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-87643 | ExpressionAtlas | 2020-04-06
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-87643-analysis-methods.tsv | Tabular | |||
| E-GEOD-87643-analytics.tsv | Tabular | |||
| E-GEOD-87643-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-87643-configuration.xml | Xml | |||
| E-GEOD-87643-g21_g1-mvaPlot.png | Other |
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Project description:O antigen acts as a shield to delay early plant immune recognition of the pathogenic bacterium, Xylella fastidiosa
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Project description:PAMP-triggered immunity (PTI) is the first line of plant defense against invading organisms. Initiated through the perception of conserved pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide or flagellin, PTI can provide early protection against a broad range of pathogens. Active suppression of PTI by microbial effector proteins, particularly those secreted by the Type III secretion system (T3SS), is a well-known strategy employed by bacterial plant pathogens that enables them to subvert PTI and successfully colonize their hosts. In this study, we demonstrate that the xylem-limited bacterium, Xylella fastidiosa, which lacks a T3SS, utilizes an alternative strategy to delay elicitation of innate immune responses. By decorating its LPS PAMP molecule with a high molecular weight O antigen, this bacterium physically masks itself from early recognition by the grapevine innate immune system. We have elucidated the chemical structure of the O antigen and found that it is primarily an α1,2-linked rhamnan polymer. X. fastidiosa cells lacking O antigen elicited hallmarks of PTI such as ROS production, specifically in the plant xylem tissue compartment, which is comprised primarily of non-living cells. By coupling histological and genome-wide transcriptional profiling, we demonstrate that X. fastidiosa lacking its O antigen shield activates defense-related genes in grapevine. This includes a stronger and more prolonged oxidative burst at concentrations high enough to inhibit pathogen proliferation. To begin exploring translational applications of our findings, we also demonstrate that purified X. fastidiosa LPS elicitor can prime grapevine defenses, thereby conferring host tolerance to subsequent challenge with X. fastidiosa.
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Project description:Tumors express a wide variety of both mutated and non-mutated antigens. Whether these tumor antigens are broadly recognized as âselfâ or âforeignâ by the immune system is currently unclear. Using an autochthonous prostate cancer model in which hemagglutinin (HA) is specifically expressed in the tumor (ProHA x TRAMP mice), as well as an analogous model wherein HA is expressed in normal tissues as a model self-antigen (C3HAHigh), we examined the transcriptional profile of CD4 T cells undergoing antigen-specific division. Consistent with our previous data, transfer of antigen-specific CD4 T cells into C3HAHigh resulted in a functionally inactivated CD4 T cell profile. Conversely, adoptive transfer of an identical CD4 T cell population into ProHA x TRAMP resulted in the induction of a regulatory phenotype (Treg) both at the transcriptional and functional level. Interestingly, this Treg skewing was a property of even early-stage tumors, suggesting Treg induction as an important tolerance mechanism during tumor development. The goal of this microarray is to detail the transcriptional profile differences between CD4 T cells that recognize their cognate antigen in the context of tumor (ProHA x TRAMP model) or self-antigen recognition (C3HA) or viral-antigen recognition (VaccHA) models or unprimed naïve state (Nontransgenic). The comparison contains both upregulated and downregulated transcripts. Experiment Overall Design: TCR transgenic CD4 T cells specific for hemagglutinin (HA) were adoptively transferred into tumor-antigen recognition model (ProHA x TRAMP), Self-antigen recognition model (C3HA), viral-antigen recognition model (VaccHA), and naïve control (Nontrangenic). Divided (CFSE diluted) CD4 T cells were sorted by FACS, RNA was extracted, and biological replicated were hybridized to an Affymetrix Mouse 430 Plus 2 expression array, followed by interrogation with an Affymetrix GeneChip Scanner 3000. RMA normalization was employed to identify differentially expressed transcripts.
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Helicobacter pylori colonizes half of the world's population as the dominant member of the gastric microbiota resulting in a lifelong chronic infection. Host responses toward the bacterium can result in asymptomatic, pathogenic or even favorable health outcomes; however, mechanisms underlying the dual role of H. pylori as a commensal versus pathogenic organism are not well characterized. Recent evidence suggests mononuclear phagocytes are largely involved in shaping dominant immunity during infection mediating the balance between host tolerance and succumbing to overt disease. We combined computational modeling, bioinformatics and experimental validation in order to investigate interactions between macrophages and intracellular H. pylori. Global transcriptomic analysis on bone marrow-derived macrophages (BMDM) in a gentamycin protection assay at six time points unveiled the presence of three sequential host response waves: an early transient regulatory gene module followed by sustained and late effector responses. Kinetic behaviors of pattern recognition receptors (PRRs) are linked to differential expression of spatiotemporal response waves and function to induce effector immunity through extracellular and intracellular detection of H. pylori. We report that bacterial interaction with the host intracellular environment caused significant suppression of regulatory NLRC3 and NLRX1 in a pattern inverse to early regulatory responses. To further delineate complex immune responses and pathway crosstalk between effector and regulatory PRRs, we built a computational model calibrated using time-series RNAseq data. Our validated computational hypotheses are that: 1) NLRX1 expression regulates bacterial burden in macrophages; and 2) early host response cytokines down-regulate NLRX1 expression through a negative feedback circuit. This paper applies modeling approaches to characterize the regulatory role of NLRX1 in mechanisms of host tolerance employed by macrophages to respond to and/or to co-exist with intracellular H. pylori.
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