Tuberculosis

Research results from P. Schierloh and co-authors update knowledge of tuberculosis

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"We show that the whole bacterium is the best inducer of IFN-gamma, although a high-molecular-weight fraction of culture filtrate proteins from M. tuberculosis H37Rv and the whole-cell lysate also induce its expression. The mannose receptor seems to mediate the inhibitory effect of mannosylated lipoarabinomannan, and Toll-like receptor 2 and 4 agonists activate NK cells but do not induce IFN-gamma like M. tuberculosis does. Antigen-presenting cells (APC) and NK cells bind M. tuberculosis, and although interleukin-12 is required, it is not sufficient to induce IFN-gamma expression, indicating that NK cell-APC contact takes place. Indeed, major histocompatibility complex class I, adhesion, and costimulatory molecules as well as NK receptors regulate IFN-gamma induction. The signaling pathway is partially inhibited by dexamethasone and sensitive to Ca2+ flux and cyclosporine. Inhibition of p38 and extracellular-regulated kinase mitogen-activated protein kinase pathways reduces the number of IFN-gamma+ NK cells. Phosphorylated p38 (p-p38) is detected in ex vivo PF-NK cells, and M. tuberculosis triggers p-p38 in PF-NK cells at the same time that binding between NK and M. tuberculosis reaches its maximum value," wrote P. Schierloh and colleagues, .

The researchers concluded: "Thus, interplay between M. tuberculosis and NK cells/APC triggering IFN-gamma would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a type 1 profile."

Schierloh and colleagues published their study in Infection and Immunity (Mycobacterium tuberculosis-induced gamma interferon production by natural killer cells requires cross talk with antigen-presenting cells involving Toll-like receptors 2 and 4 and the mannose receptor in tuberculous pleurisy. Infection and Immunity, 2007;75(11):5325-37).

For more information, contact P. Schierloh, Instituto de Investigaciones Hematologicas, Departamento de Inmunologia, Academia Nacional de Medicina, Buenos Aires, Argentina.

Publisher contact information for the journal Infection and Immunity is: American Society Microbiology, 1752 N St. NW, Washington, DC 20036-2904, USA.

Keywords: Argentina, Buenos Aires, Cutaneous Tuberculosis, Interferon, Mycobacteria, Mycobacterium Tuberculosis, Pleurisy.

This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2007, Biotech Business Week via NewsRx.com.