Molecular profiling of the tuberculin skin test in patients with active tuberculosis with and without HIV-1 co-infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Mahdad Noursadeghi
PROVIDER: E-MTAB-3254 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Whole genome transcriptional profiling of punch biopsies from the site of 2U intradermal tuberculin or equivalent volume of saline injection at 48 hours after injection in patients that have been cured of active tuberculosis (TB) disease.
2019-05-01 | E-MTAB-6815 | biostudies-arrayexpress
Project description:Whole genome transcriptional profiling of punch biopsies from the site of 2U intradermal tuberculin or equivalent volume of saline injection at 48 hours after injection in individuals that have been cured of active tuberculosis disease.
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Project description:Transcriptome at the site of a 48 hour tuberculin skin test (TST) and saline injection from patients with active TB disease and latent TB infection
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Project description:Anti-TNF therapy has transformed the management of rheumatoid arthritis (RA); however little is known about its effects on cell mediated immune responses and TNF-inducible activity at the site of inflammation. Here, we used the tuberculin skin test (TST) as a standardised in vivo human challenge model to make systems level assessments of the effects of anti-TNF therapy in a prototypic cell mediated immune response. RA patients (treated with monoclonal anti-TNF antibodies (adalimumab or infliximab), the soluble TNF receptor etanercept or the standard therapy methotrexate) and healthy volunteers with immunological memory to Mycobacterium tuberculosis antigens were identified using an interferon-γ release assay of peripheral blood. Two units tuberculin or an equivalent volume of saline was injected into the forearm of study participants (n=50). After 72 hours, 3 mm skin punch biopsies were taken from the injection site and processed for whole genome transcriptional profiling by Agilent gene microarray.
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Project description:Transcriptional profiling of biopsies from tuberculin skin test sites was performed to investigate the interaction of complex cellular and molecular networks at the interface between innate and adaptive immunity which coordinate anti-mycobacterial responses in vivo.
2012-05-13 | E-TABM-1157 | biostudies-arrayexpress
Project description:Understanding mechanisms of resistance to M. tuberculosis (M.tb) infection in humans could identify novel therapeutic strategies as it has for other infectious diseases. We hypothesized that monocytes from household contacts of pulmonary tuberculosis patients that failed to convert their tuberculin skin tests (TSTNEG) would respond differently to M.tb infection when compared to matched tuberculin skin test positive controls (TSTPOS). We obtained genome-wide transcriptional profiles of M.tb-infected peripheral blood monocytes from 10 TSTNEG and 18 TSTPOS Ugandans. We used Gene Set Enrichment Analysis and interaction networks to identify cellular processes associated with TST status. We discovered gene sets associated with histone deacetylases that were differentially expressed when comparing TSTPOS and TSTNEG subjects. We used small molecule inhibitors to demonstrate that histone deacetylase function is important for the pro-inflammatory response to M.tb infection in monocytes. Monocytes from individuals who appear to resist M.tb infection differentially activate pathways controlled by histone deacetylase in response to M.tb infection when compared to those who are susceptible to infection. These data identify a potential cellular mechanism underlying the clinical phenomenon of persistently negative tuberculin skin tests despite known exposure to an infectious contact.
2016-01-15 | GSE76873 | GEO
Project description:The primary goal of this project is to monitor host global gene expression patterns in response to viral infection in the shrimp, Litopenaeus stylirostris. Specific Pathogen Free (SPF) L. stylirostris were obtained from High Health Aquaculture (Honolulu, Hawaii) and kept in environmentally controlled tanks. For control, animals were injected with saline (30 ul) between the second and third tergal plates of the lateral side of the tail using a 1 ml tuberculin syringe. Infected individuals were inoculated with homogenate created from IHHNV infected shrimp tissue. After 24 hours, the shrimp were sacrificed and tissue was collected from the ventral and flash frozen in liquid nitrogen and stored in the -80 ºC freezer. Libraries of sequence tags were generated via the Long-SAGE kit (Invitrogen®, Carlsbad, CA) until the ditag PCR preparation step and directly pyrosequenced by 454 Roche.
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Project description:Understanding mechanisms of resistance to M. tuberculosis (M.tb) infection in humans could identify novel therapeutic strategies as it has for other infectious diseases. We hypothesized that monocytes from household contacts of pulmonary tuberculosis patients that failed to convert their tuberculin skin tests (TSTNEG) would respond differently to M.tb infection when compared to matched tuberculin skin test positive controls (TSTPOS). We obtained genome-wide transcriptional profiles of M.tb-infected peripheral blood monocytes from 10 TSTNEG and 18 TSTPOS Ugandans. We used Gene Set Enrichment Analysis and interaction networks to identify cellular processes associated with TST status. We discovered gene sets associated with histone deacetylases that were differentially expressed when comparing TSTPOS and TSTNEG subjects. We used small molecule inhibitors to demonstrate that histone deacetylase function is important for the pro-inflammatory response to M.tb infection in monocytes. Monocytes from individuals who appear to resist M.tb infection differentially activate pathways controlled by histone deacetylase in response to M.tb infection when compared to those who are susceptible to infection. These data identify a potential cellular mechanism underlying the clinical phenomenon of persistently negative tuberculin skin tests despite known exposure to an infectious contact. CD14+ monocytes from 18 TSTPOS and 10 TSTNEG subjects were isolated by positive selection. Depending on the yield, between 5E5 and 1E6 monocytes were plated in duplicate in a 24-well tissue culture plate and rested overnight at 37oC, 5% CO2. The next day, cells were mock-infected or infected with virulent M. tuberculosis strain H37Rv at a multiplicity of infection (MOI) 10:1. After a six hour incubation at 37C, 5% CO2, the mycobacteria were killed and total RNA harvested using TRIzol-LS (Invitrogen). TRIzol samples were stored at -80oC until all infections were completed. To minimize batch effects, equal numbers of TSTPOS and TSTNEG subjects were processed on each of six days and frozen aliquots of M.tb were used for infections. RNA was extracted using the RNeasy Mini Kit with on-column DNAse digestion. RNA was transcribed into complementary DNA, labeled, and hybridized onto Illumina HT-12 microarrays according to the manufacturerâs instructions. Probe intensities were quantified using Illumina iScan platform and processed using BeadArray without performing normalization or background correction.
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Project description:Psoriasis is a chronic, debilitating, immune-mediated inflammatory skin disease. As IFN-gamma is involved in many cellular processes, including activation of T cells and dendritic cells (DCs), antigen processing and presentation, cell adhesion and trafficking, and cytokine and chemokine production, IFN-gamma-producing Th1 cells were proposed to be integral to the pathogenesis of psoriasis. Recently, IFN-gamma was shown to enhance IL-23 and IL-1 production by DCs and subsequently induce Th17 cells, important contributors to the inflammatory cascade in psoriasis lesions. To determine if IFN-gamma indeed induces the pathways leading to the development of psoriasis lesions, a single intradermal injection of IFN-gamma was administered to an area of clinically normal, non-lesional skin of psoriasis patients and biopsies were collected 24 hours later. Although there were no visible changes in the skin, IFN-gamma induced molecular and histological features characteristic of psoriasis lesions. IFN-gamma increased a number of differentially expressed genes in the skin, including many chemokines concomitant with an influx of T cells and inflammatory DCs. Furthermore, inflammatory DC products TNF, iNOS, IL-23, and TRAIL were present in IFN-gamma-treated skin. Thus, IFN-gamma, which is significantly elevated in non-lesional skin compared to healthy skin, appears to be a key pathogenic cytokine that can induce the inflammatory cascade in psoriasis. RNA was isolated from whole skin punch biopsies of either healthy or non-lesional psoraisis patients at baseline or 24 hours after placebo or IFN-g injection.
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