Fig. 10.
Fig. 10. Tissue sections were prepared from kidneys of wild-type, G-CSF−/−, and G-CSF−/−/GM-CSF−/− mice 7 days after infection with C albicans. / Sections were stained with Gomori methenamine silver stain (top panel) and haematoxylin-eosin stain (bottom panel). (A, D) Wild-type mice show healing inflammatory lesions in the cortex and few yeast cells. (B-C, E-F) G-CSF–deficient and G-CSF/GM-CSF-deficient mice, respectively, show numerous abscesses throughout the section with large aggregates of fungal yeasts within abscesses. Inset shows polymorphonuclear neutrophils in an area of dense leukocytic infiltration surrounding fungal yeasts (marked by arrows).

Tissue sections were prepared from kidneys of wild-type, G-CSF−/−, and G-CSF−/−/GM-CSF−/− mice 7 days after infection with C albicans.

Sections were stained with Gomori methenamine silver stain (top panel) and haematoxylin-eosin stain (bottom panel). (A, D) Wild-type mice show healing inflammatory lesions in the cortex and few yeast cells. (B-C, E-F) G-CSF–deficient and G-CSF/GM-CSF-deficient mice, respectively, show numerous abscesses throughout the section with large aggregates of fungal yeasts within abscesses. Inset shows polymorphonuclear neutrophils in an area of dense leukocytic infiltration surrounding fungal yeasts (marked by arrows).

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