Volume 18, Issue 3 (Aug/Sep 2010)                   JSSU 2010, 18(3): 271-276 | Back to browse issues page

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Abstract:   (9199 Views)
Introduction: Mycobacterium ulcerans is the etiological agent of Buruli ulcer (BU) the third most common mycobacterial infection in humans after tuberculosis and leprosy. BU is now considered by the WHO to be an emerging infection of major concern. M. ulcerans produces mycolactone toxin, which is required for the organism’s virulence. Mycolactone destroys tissue and suppresses host immune responses. Methods: In this descriptive analytical study, peripheral blood mononuclear cells from three volunteers with no history of buruli ulcer were used. IL-6 and TNF produced by these cells at different preincubation times with LPS and mycolactone were measured by using ELISA kits. Results: This study showed hyper inhibition of IL-6 and TNF production by mycolactone. TNF levels in the control tubes (containing LPS) in 4hours reached its maximum value and then decreased. While the production of IL-6 in the tube with fresh cells (zero time) had the highest value, after 16hours, it reached its minimum. Conclusion: Since TNF and IL-6 are important immunity inflammatory cytokines, it can be well imagined that decrease of TNF production by this bacterium plays a role in weakening of inflammatory response. So Mycobacterium ulcerans destroys macrophages and at the same time prevents TNF production by important cells in innate immune mechanism.
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Type of Study: Original article | Subject: General
Received: 2010/08/10 | Published: 2010/08/15

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