The role of toll-like receptor (TLR) 2 and TLR4 in the host defense against disseminated candidiasis.
until further notice
SourceThe Journal of Infectious Diseases, 185, 10, (2002), pp. 1483-1489
Article / Letter to editor
Display more detailsDisplay less details
The Journal of Infectious Diseases
SubjectThe role of cytokines in the pathophysiology of febrile illnesses and in host defense against infections; De rol van cytokinen in de pathofysiologie van koortsende ziekten en in de afweer tegen infecties
Toll-like receptors (TLRs) represent the main class of pattern-recognition receptors involved in sensing pathogenic microorganisms. The aim of the present study was to assess the role of TLR4 in the defense against Candida albicans infection. The outgrowth of C. albicans was 10-fold higher in TLR4-defective C3H/HeJ mice, compared with that in control C3H/HeN mice (P<.05). Production of tumor necrosis factor (TNF) and interleukin (IL)-1alpha and IL-1beta by mouse macrophages in response to C. albicans stimulation was not affected by TLR4, and the candidacidal capacities of the neutrophils and macrophages of C3H/HeJ mice were normal. In contrast, production of the CXC chemokines KC and macrophage inhibitory protein-2 was 40%-60% lower by the macrophages of C3H/HeJ mice (P<.05), which resulted in a 40% decrease in neutrophil recruitment to the site of infection. Candida-induced TNF and IL-1beta production by human peripheral blood mononuclear cells was significantly inhibited by blocking anti-TLR2 antibodies in vitro. In conclusion, TLR4-defective C3H/HeJ mice are more susceptible to C. albicans infection, and this is associated with impaired chemokine expression and neutrophil recruitment.
Upload full text
Use your RU credentials (u/z-number and password) to log in with SURFconext to upload a file for processing by the repository team.