showing 3 related works from this author
Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis
2004
Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…
TLR2: for or against Candida albicans?
2005
In a recent issue of Trends in Microbiology, Netea and coworkers presented their opinion that toll-like receptors (TLRs) are involved in escape from the defense mechanisms of the host [1]. In their article, the authors clearly identified three major TLR-mediated escape mechanisms that are used by microbial pathogens, such as Yersinia, Mycobacterium and Candida. Here, we wish to comment on the roll of TLR2 in Candida albicans infections. Netea's interesting hypothesis, that TLR2 expression might confer to mice an increased susceptibility to C.
Toll-like receptor-2 is essential in murine defenses against Candida albicans infections
2004
In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity…