Fungal Iron Availability during Deep Seated Candidiasis Is Defined by a Complex Interplay Involving Systemic and Local Events
Figure 5
Systemic candidiasis disturbs host renal iron homeostasis and affects splenic function.
Panels A–C. Immunohistochemical detection of iron homeostasis associated proteins in kidneys of healthy and infected animals reveals correlation with renal iron loading. Ferritin, HO-1, HO-2, and the transferrin receptor (TfR) all increase in infected kidneys in comparison to healthy controls (A) Ferritin is distributed outside areas occupied by C. albicans (A, arrowheads). In healthy tissue (B, left), ferritin content is low and mainly cortical, while increased and mainly medullary in animals with advanced candidiasis (B, right). HO-1 is concentrated in rings encompassing fungal lesions (A, arrowheads) and is produced by cell type(s) other than the Ly-6G or F4/80-producing immune cells (C). Panel D. Immunohistochemical analyses of murine spleens. Blue areas correspond to white pulp (dotted lines), embedded in the red pulp. Red pulp macrophages stain selectively with anti-HO-1 and anti-F4/80 antibodies: the stain for HO-1 is depleted in tissues from infected animals (arrows) (D). In all cases, the experiments represent C. albicans SC5314 infections in BALB/c mice. ‘Pas_h’, sections processed for histology; ‘c’, kidney cortex; ‘m’, medulla; ‘control’, experimental control with no primary antibodies. Size bars: panels A and D, 500 µm; B, 1000 µm; C, 200 µm.