Figure 1.
Cryptococcal trehalose phosphate synthase 1 (tps1) gene deletion enables rapid reduction of pulmonary fungal burden via a T-cell-independent mechanism. C57BL/6 and BALB/c mice were infected intratracheally (IT) with 1*105 WT (H99), tps1 KO (tps1Δ), or complemented (tps1Δ:TPS1) C. neoformans (Cn). (A) The Cn-infected mice were monitored for 28 days postinfection (dpi) for survival. All the H99-infected mice reached endpoint criteria between 14 dpi and 25 dpi, whereas all tps1Δ-infected mice survived. Data from a matched experiment; n = 5 mice/group. (B) Pulmonary fungal burdens were evaluated at 1 dpi, 3 dpi, and 7 dpi. Data are pooled from at least three matched experiments (n = 2–6 mice/group). (C) Lung fungal burdens at 3 dpi in tps1Δ-infected BALB/c mice treated with anti-CD4 depleting antibody or control (PBS) injections. Data from two pooled experiments; n = 2–5 mice/group. Data in all figures are the means ± SEM (unless otherwise indicated) and analyzed as described in the methods section. Statistically significant differences are indicated in all figures as follows: *p ≤ 0.05, **p ≤ 0.01, ****p ≤ 0.0001. NS, no significance.