Figure 2.

Decreased inflammation in the lungs of interleukin-1 receptor type I-deficient (IL-1RI^−/−) mice following infection with Cryptococcus neoformans 52D. Wild-type (WT) and IL-1RI^−/− mice were infected intratracheally with 10⁴ CFU of C. neoformans 52D. Lungs were harvested at day 35 postinfection; perfused with phosphate-buffered saline; embedded in paraffin; and stained with hematoxylin–eosin (H&E), mucicarmine, or periodic acid–Schiff (PAS). Representative H&E images (A) show a significant reduction of inflammation in IL-1RI^−/− compared to WT mice; the black arrow points to eosinophilic crystals in IL-1R^−/− lung. Mucicarmine staining (B) shows numerous heavily encapsulated extracellular C. neoformans in the airspaces of IL-1RI^−/− mice compared to WT mice. Representative images of lungs stained with PAS (C) show goblet cell hyperplasia and mucus in the airways of infected IL-1RI^−/− mice compared to WT mice. Each image is representative of 100 fields examined (n = 4 mice/strain from two independent experiments).