Despite advances in diagnosis and treatment, Mycobacterium tuberculosis causes active disease in about 8 million people worldwide annually. The study of the interplay between the host and the pathogen at the site of infection in human TB may contribute to elucidate the pathogenesis of the disease. In this work, using macroarray technology and real-time PCR, we analyzed the modulation of 847 genes encoding immune-inflammatory mediators in BALF samples of patients affected by active pulmonary TB (PTB) and control patients affected by non-TB diseases. The data show that the PTB milieu contains a complex network of gene activation. Different genes with adhesive properties and involved in tissue repair and fibrosis were modulated. In TB patients, we observed the up-regulation of cytokines, including IFN-gamma and IFN-gamma pathway genes, of several apoptotic genes, and of potent transcriptional activators. These findings can contribute to elucidate the mechanisms of MTB pathogenicity in humans. (c) 2006 Elsevier Inc. All rights reserved.

Grassi, M., Bocchino, M., Marruchella, A., Volpe, E., Saltini, C., Colizzi, V., et al. (2006). Transcriptional profile of the immune response in the lungs of patients with active tuberculosis. CLINICAL IMMUNOLOGY, 121(1), 100-107 [10.1016/j.clim.2006.06.008].

Transcriptional profile of the immune response in the lungs of patients with active tuberculosis

SALTINI, CESARE;COLIZZI, VITTORIO;
2006-01-01

Abstract

Despite advances in diagnosis and treatment, Mycobacterium tuberculosis causes active disease in about 8 million people worldwide annually. The study of the interplay between the host and the pathogen at the site of infection in human TB may contribute to elucidate the pathogenesis of the disease. In this work, using macroarray technology and real-time PCR, we analyzed the modulation of 847 genes encoding immune-inflammatory mediators in BALF samples of patients affected by active pulmonary TB (PTB) and control patients affected by non-TB diseases. The data show that the PTB milieu contains a complex network of gene activation. Different genes with adhesive properties and involved in tissue repair and fibrosis were modulated. In TB patients, we observed the up-regulation of cytokines, including IFN-gamma and IFN-gamma pathway genes, of several apoptotic genes, and of potent transcriptional activators. These findings can contribute to elucidate the mechanisms of MTB pathogenicity in humans. (c) 2006 Elsevier Inc. All rights reserved.
2006
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/10 - MALATTIE DELL'APPARATO RESPIRATORIO
English
Con Impact Factor ISI
BALF; Host-pathogen interaction; Immune response; Inflammatory cytokine genes; Macroarray; Mycobacterium tuberculosis; Site of infection
cytokine; gamma interferon; adult; apoptosis; article; bacterial virulence; cellular immunity; clinical article; controlled study; cytokine production; disease course; disease severity; DNA microarray; female; gene activation; gene function; genetic regulation; genetic transcription; human; human cell; immune response; immunogenetics; immunopathogenesis; inflammation; lung fibrosis; lung lavage; lung tuberculosis; male; Mycobacterium tuberculosis; priority journal; real time polymerase chain reaction; tissue repair; transcription initiation; upregulation; Adult; Cells, Cultured; Female; Gene Expression Profiling; Humans; Male; Middle Aged; Mycobacterium tuberculosis; Oligonucleotide Array Sequence Analysis; Polymerase Chain Reaction; Pulmonary Alveoli; RNA, Messenger; Transcription, Genetic; Tuberculosis, Pulmonary
Grassi, M., Bocchino, M., Marruchella, A., Volpe, E., Saltini, C., Colizzi, V., et al. (2006). Transcriptional profile of the immune response in the lungs of patients with active tuberculosis. CLINICAL IMMUNOLOGY, 121(1), 100-107 [10.1016/j.clim.2006.06.008].
Grassi, M; Bocchino, M; Marruchella, A; Volpe, E; Saltini, C; Colizzi, V; Mariani, F
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/56963
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