Related Experiment Videos
Normal host defense during systemic candidiasis in mannose receptor-deficient mice
Sena J Lee1, Nai-Ying Zheng, Monica Clavijo
1Laboratory of Molecular Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10021, USA.
Infection and Immunity
|December 24, 2002
Summary
The mannose receptor (MR) does not play a crucial role in fighting systemic Candida albicans infections in mice. Immune responses and survival were similar between MR-deficient and wild-type mice.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Pathogen pattern recognition receptors (PRRs) are vital for innate immunity.
- The mannose receptor (MR) is a PRR implicated in phagocytosis of microbes like Candida albicans.
- The MR's role in systemic C. albicans infection immunity is not well-defined.
Purpose of the Study:
- To investigate the in vivo role of the MR in host defense during disseminated candidiasis.
- To determine if MR deficiency impacts survival, fungal burden, and immune cell responses to C. albicans.
Main Methods:
- MR-deficient (MR-/-) and wild-type mice were infected intraperitoneally with C. albicans.
- Evaluated survival rates, tissue fungal burden, inflammatory cell recruitment, and antibody production.
- In vitro experiments assessed C. albicans uptake by MR-/- macrophages.
Main Results:
- No significant difference in survival was observed between MR-/- and wild-type mice.
- MR-/- mice showed higher fungal burdens in some organs at later time points but maintained immune cell recruitment and antibody production.
- In vitro, MR-/- macrophages exhibited normal C. albicans uptake, which could be inhibited by beta-glucan.
Conclusions:
- The MR is not essential for host defense against disseminated candidiasis.
- The MR is not required for C. albicans phagocytosis by macrophages.
- A beta-glucan receptor may be critical for C. albicans phagocytosis.