Galectin-3 plays an important role in protection against disseminated candidiasis

Abstract

Recent in vitro studies have implicated galectin-3 as an important receptor in host recognition and response to specific Candida species; however its role in protection against disseminated candidiasis in vivo has not been evaluated. This study investigated the importance of galectin-3 in host defense against systemic infection with the highly virulent species Candida albicans (C. albicans), and the less virulent species, Candida parapsilosis (C. parapsilosis). Mice deficient in galectin-3 (gal3−/−) were more susceptible to infection than wild type (WT) mice. When infected with C. albicans, gal3−/− mice died significantly faster and exhibited a trend towards increased fungal burden and increased abscess formation in infected brains compared to WT mice. When infected with C. parapsilosis, gal3−/− mice had significantly higher renal fungal burdens and abscess formation compared to WT mice. To evaluate whether galectin-3 may contribute to susceptibility to candidiasis in human infants, galectin-3 levels in sera of newborn infants, a patient population uniquely susceptible to infections with both C. albicans and C. parapsilosis, were compared to serum galectin-3 levels of adults. Galectin-3 levels were significantly lower in newborn infant sera compared to adult sera. These data indicate that galectin-3 plays an important role in a murine model of disseminated candidiasis and suggest a potential mechanism of neonatal susceptibility to these infections.

The role of pattern recognition receptors in the innate recognition ofCandida albicans

“…More specifically, gal3-/-mice died significantly faster and exhibited a trend toward increased fungal burden and increased abscess formation in infected brains compared to WT mice. 186 [198,170] NLRP3 has been found critical for the control of C. albicans infections. 35 Mice deficient in NLRP3 displayed diminished serum IL-1b, reduced survival and higher fungal burdens in kidney, spleen, liver, and lung upon C. albicans infection.…”

The Cek1‑mediated MAP kinase pathway regulates exposure of α‑1,2 and β‑1,2‑mannosides in the cell wall ofCandida albicansmodulating immune recognition

“…These results are unexpected as it was reported that mice defective in galectin-3 are more sensitive to C. albicans infection. 81,82 While we do not have an explanation for this, differences could exist between both set of experiments regarding the infectious dose used and the origin of the used galectin-3 C/C and galectin-3 ¡/¡ mice (our strain is backcrossed for over 9 generations to C57BL/7 mice while this number is lower in commercial (Jackson Laboratories) mice) that could be maybe responsible for the observed discrepancies. Nevertheless, an increased resistance of galectin-3 null mice has been also observed in infections with Trypanosoma brucei, 83 Salmonella…”

Genetic, transcriptome, proteomic and epidemiological evidence for blood brain barrier disruption and polymicrobial brain invasion as determinant factors in Alzheimer’s disease

“…It is made available under a The copyright holder for this preprint (which was not . http://dx.doi.org/10.1101/080333 doi: bioRxiv preprint first posted online Oct. 12, 2016; C.Albicans infection [169].…”