Production of Interleukin-18 in Human Tuberculosis

• Published in: The Journal of infectious diseases Vol. 182; no. 1; pp. 234 - 239
• Main Authors: Vankayalapati, Rhea Ramakrishna, Wizel, Benjamin, Weis, Stephen E., Samten, Buka, Girard, William M., Barnes, Peter F.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.07.2000; University of Chicago Press; Oxford University Press
• Subjects: Bacterial diseases; Biological and medical sciences; Cytokines; Fungal diseases; Fungal infections; Human bacterial diseases; Humans; In Vitro Techniques; Infections; Infectious diseases; Interferon-gamma - metabolism; Interleukin-18 - biosynthesis; Interleukin-2 - metabolism; Leukocytes, Mononuclear - metabolism; Leukocytes, Mononuclear - microbiology; Macrophages, Alveolar - metabolism; Major Articles; Medical sciences; Monocytes; Mycobacterium tuberculosis; Mycobacterium tuberculosis - immunology; Mycobacterium tuberculosis - physiology; Pleural tuberculosis; T lymphocytes; Tuberculin; Tuberculosis; Tuberculosis - immunology; Tuberculosis and atypical mycobacterial infections; Human; Immunoprotection; Respiratory disease; Cytokine; Host agent relation; Mycobacterial infection; Interleukin 18; Infection; Tuberculosis; Mycobacterium tuberculosis; Mycobacteriales; Bacteriosis; Mycobacteriaceae; Bacteria; Actinomycetes; Gamma interferon
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/315656

To investigate the role of interleukin (IL)-18 in human tuberculosis, IL-18 production was evaluated in blood and at the site of disease in patients with tuberculosis. Mycobacterium tuberculosis-stimulated peripheral blood mononuclear cells (PBMC) from tuberculosis patients secreted less IL-18 and interferon-γ (IFN-γ) than did PBMC from healthy persons reactive to tuberculin. M. tuberculosis-induced IFN-γ production was inhibited by anti-IL-18 and enhanced by recombinant IL-18. Alveolar macrophages secreted IL-18 in response to M. tuberculosis, and IL-18 and IFN-γ concentrations were higher in pleural fluid of patients with tuberculosis than in pleural fluid of patients with nontuberculous diseases. These findings demonstrate that IL-18 production by PBMC correlates with IFN-γ production and effective immunity to tuberculosis, suggesting that IL-18 contributes to a protective type 1 cytokine response in persons with mycobacterial infection.