Gene Expression Analysis of Blood PBMC Response to Mycobacterium leprae antigens
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE179987 | GEO | 2021/07/16
REPOSITORIES: GEO
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Project description:Leprosy is classified from paucibacillary leprosy (TT and BT) to multibacillary leprosy (BB, BL, and LL). In our study, we focus on selecting or classfying the significant genes to discriminate between paucibacillary and multibacillary group and the important genes to distinguish between blood and the corresponding tissue in patients.
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Project description:Leprosy is classified from paucibacillary leprosy (TT and BT) to multibacillary leprosy (BB, BL, and LL). In our study, we focus on selecting or classfying the significant genes to discriminate between paucibacillary and multibacillary group and the important genes to distinguish between blood and the corresponding tissue in patients. · Human Adult Normal Skin Sample (Commercial;Cat#1234218); 6 patients of leprosy (Blood and Tissue sample (Pathologic classification: BT); 6 patients of leprosy (Blood and Tissue sample (Pathologic classification: MB)) · In blood sample, BT sample vs MB sample · In tissue sample, Normal Skin sample vs tissue BT sample or tissue MB sample · Single Color Microarray · All experiments are performed one replicate
2011-03-17 | E-GEOD-24280 | biostudies-arrayexpress
Project description:Leprosy is a human infectious disease caused by Mycobacterium leprae. A strong host genetic contribution to leprosy susceptibility is well established. However, the modulation of the transcriptional response to infection and the mechanism(s) of disease control are poorly understood. To address this gap in knowledge of leprosy pathogenicity, we conducted a genome-wide search for expression quantitative trait loci (eQTL) that are associated with transcript variation –– before and after stimulation with M. leprae sonicate in whole blood cells. We show that M. leprae antigen stimulation mainly triggered the upregulation of immune related genes and that a substantial proportion of the differential gene expression is genetically controlled. Indeed, using stringent criteria, we identified 318 genes displaying cis-eQTL at an FDR of 0.01, including 66 genes displaying response-eQTL (reQTL), i.e. cis-eQTL that showed significant evidence for interaction with the M. leprae stimulus. Such reQTL correspond to regulatory variations that affect the interaction between human whole blood cells and M. leprae sonicate, and thus likely between the human host and M. leprae bacilli. We found that reQTL are significantly enriched among binding sites of transcription factors that are activated in response to infection, and that they were enriched among single nucleotide polymorphisms (SNPs) associated with susceptibility to leprosy per se and Type-I Reaction, as well as SNPs targeted by recent positive selection. Our study suggests that natural selection shaped our genomic diversity to face pathogen exposure including M. leprae infection.
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Project description:The initial interaction between a microbial pathogen and the host immune response influences the outcome of the battle between the host and the foreign invader. Leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, provides a model to study relevant human immune responses. Previous studies have adopted a targeted approach to investigate host response to M. leprae infection, focusing on the induction of specific molecules and pathways. By measuring the host transcriptome triggered by M. leprae infection of human macrophages, we were able to detect a host gene signature 24–48 hours after infection characterized by specific innate immune pathways involving the cell fate mechanisms autophagy and apoptosis. The top upstream regulator in the M. leprae-induced gene signature was NUPR1, which is found in the M. leprae-induced cell fate pathways. The induction of NUPR1 by M. leprae was dependent on the production of the type I interferon (IFN), IFN-β. Furthermore, NUPR1 mRNA and protein were upregulated in the skin lesions from patients with the multibacillary form of leprosy. Together, these data indicate that M. leprae induces a cell fate program which includes NUPR1 as part of the host response in the progressive form of leprosy
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