Fig 5.

ATG5 conditional knockout alters the murine immune response to intratracheal C. neoformans infection. (A to C) Histology of the lungs of ATG5-conditional-knockout and control mice 3, 7, and 14 days after intratracheal infection with 10⁵ C. neoformans cells. Hematoxylin-eosin-stained sections were evaluated semiquantitatively by a veterinary pathologist. Five mice were used per group per time interval. (A) The arrow points to a reactive vessel. (B) The arrows point to infiltrated neutrophils with dense polymorphic nuclei and scant cytoplasm, whereas the arrowheads indicate infiltrated macrophages with round nuclei and large cytoplasm. (C) The arrowheads point to alveoli that are not occupied by C. neoformans or inflammatory cells in the lungs of conditional-knockout mice. (D) Macroscopic appearance of the lungs from 3 ATG5-conditional-knockout mice and 3 control mice infected with C. neoformans for 14 days showing large translucent nodules in the controls and smaller tan-red nodules in the ATG5-conditional-knockout animals. (E) IHC localization of Ym-1, a marker of alternatively activated macrophages, on lung sections from days 3 and 14. The arrows point to clusters of alternatively activated macrophages on the lungs of control mice infected with C. neoformans for 3 days. Bars, 500 μm (images at ×2.5 and ×4 magnifications) and 50 μm (images at ×40 magnification).