We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Local Activation of the Innate Immune System in Buruli Ulcer Lesions.
- Authors
Peduzzi, Elisabetta; Groeper, Célia; Schütte, Daniela; Zajac, Paul; Rondini, Simona; Mensah-Quainoo, Ernestina; Spagnoli, Giulio Cesare; Pluschke, Gerd; Daubenberger, Claudia Andrea
- Abstract
Buruli ulcer (BU) caused by Mycobacterium ulcerans is a chronic necrotizing disease of the skin and the underlying soft tissue. Fat tissue necrosis accompanied by minimal inflammation is considered the most reliable histopathologic feature of BU. There may be a constant influx of inflammatory cells to the sites of active infection but these are thought to be killed by mycolactone, a polyketide toxin produced by M. ulcerans, through apoptosis and necrosis. Here we describe the spatial correlations between mycobacterial load and the expression of dendritic cell (DC) surface markers (cluster of differentiation (CD)83, CD11c, and CD123), the Toll-like receptor (TLR) 9 and pro- and anti-inflammatory cytokines (IL-8, IL-6, tumor necrosis factor-alpha (TNF-α), IFN-α, IL-12p40, IL-10, and IFN-γ) within BU lesions. Although IL-8, IL-6, and TNF-α messenger RNA (mRNA) was detectable by real-time PCR in all lesions, the expression of the other cytokines was only found as small foci in some lesions. Correlations of the distribution of mRNA encoding the activation marker CD83 and the DC subset markers CD123 and CD11c indicate that both activated plasmacytoid and myeloid dendritic cells were present in the lesions. Results suggest that M. ulcerans specific immune responses may develop once therapeutic interventions have limited the production of mycolactone.Journal of Investigative Dermatology (2007) 127, 638–645. doi:10.1038/sj.jid.5700593; published online 19 October 2006
- Subjects
ULCERS; SKIN diseases; MYCOBACTERIUM; APOPTOSIS; CYTOKINES; NATURAL immunity
- Publication
Journal of Investigative Dermatology, 2007, Vol 127, Issue 3, p638
- ISSN
0022-202X
- Publication type
Article
- DOI
10.1038/sj.jid.5700593