Disseminated candidiasis and hepatic malarial infection in mannose-binding-lectin-A-deficient mice.
To examine the physiological functions of mannose-binding lectin A (MBL-A), we generated mice that were deficient in MBL-A and examined their susceptibilities to the microbial pathogens Candida albicans and Plasmodium yoelii, an accepted experimental malaria model in mouse. We found no differences in the survival rates and fungal burdens of wild-type and MBL-A(-/-) mice with disseminated C. albicans infection. The two mouse strains were also similar in their abilities to resist hepatic accumulation of P. yoelii parasites. We conclude that MBL-A deficiency does not alter resistance to disseminated candidiasis or initial hepatic invasion by P. yoelii.
Lee
Sena J
SJ
Laboratory of Molecular Immunology, The Rockefeller University. Howard Hughes Medical Institute, New York, New York 10021, USA.
Gonzalez-Aseguinolaza
Gloria
G
Nussenzweig
Michel C
MC
D000818:Animals; D002176:Candida albicans / Q000502:physiology; D002177:Candidiasis / Q000276:immunology*; D004198:Disease Susceptibility; D005091:Exons / Q000235:genetics; D006801:Humans; D008099:Liver / Q000382:microbiology* / Q000469:parasitology*; D008288:Malaria / Q000276:immunology*; D037601:Mannose-Binding Lectin / Q000031:analogs & derivatives* / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D010967:Plasmodium yoelii / Q000502:physiology
D037601:Mannose-Binding Lectin; C069858:mannose binding protein A