AI Article Synopsis
- Candidiasis is frequently seen in diabetic patients, and it has been found that complement factor H (FH) plays a significant role in the evasion of the immune response by binding to the high-affinity glucose transporter 1 (Hgt1), which is dependent on glucose levels.
- In a study involving mice, those with diabetes showed significantly higher virulence and lethality when challenged with a strain of Candida lacking Hgt1 compared to the parental strain.
- Laboratory results indicated that at high glucose concentrations, the parental strain demonstrated lower phagocytosis and higher FH deposition, but this glucose dependency has only a minor effect on phagocytosis, showing that the absence of Hgt1 alters the immune response but does not
Article Abstract
Candidiasis is common in diabetic patients. Complement evasion is facilitated by binding complement factor H (FH). Since the expression of high-affinity glucose transporter 1 (Hgt1), a FH-binding molecule, is glucose-dependent, we aimed to study its relevance to the pathogenesis of . Euglycemic and diabetic mice were intravenously challenged with either lacking Hgt1 (hgt1-/-) or its parental strain (SN152). Survival and clinical status were monitored over 14 days. In vitro, strains were grown at different glucose concentrations, opsonized with human serum, and checked for C3b/iC3b and FH deposition. Phagocytosis was studied by fluorescein isothiocyanate-labeled opsonized yeast cells incubated with granulocytes. The murine model demonstrated a significantly higher virulence of SN152 in diabetic mice and an overall increased lethality of mice challenged with hgt1-/-. In vitro lower phagocytosis and C3b/iC3b deposition and higher FH deposition were demonstrated for SN152 incubated at higher glucose concentrations, while there was no difference on hgt1-/- at physiological glucose concentrations. Despite C3b/iC3b and FH deposition being glucose-dependent, this effect has a minor influence on phagocytosis. The absence of Hgt1 is diminishing this dependency on complement deposition, but it cannot be attributed to being beneficial in a murine model.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8868559 | PMC |
| http://dx.doi.org/10.3390/antibiotics11020257 | DOI Listing |
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