The University of Sydney Marie Bashir Institute for Infectious Diseases and Biosecurity, Sydney, Australia; Fungal Pathogenesis Laboratory, Centre for Infectious Diseases and Microbiology, The Westmead Institute for Medical Research, Westmead, Australia.
The University of Sydney Marie Bashir Institute for Infectious Diseases and Biosecurity, Sydney, Australia; Fungal Pathogenesis Laboratory, Centre for Infectious Diseases and Microbiology, The Westmead Institute for Medical Research, Westmead, Australia; The Westmead Clinical School, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Am J Pathol. 2018 Jul;188(7):1653-1665. doi: 10.1016/j.ajpath.2018.03.015. Epub 2018 Jun 19.
The innate immune system is the primary defense against cryptococcal infection, but paradoxically it promotes infection of the central nervous system. We performed a detailed longitudinal study of neurocryptococcosis in normal, chimeric, green fluorescent protein phagocyte-positive mice and phagocyte-depleted mice and interrogated the central nervous system innate immune response to Cryptococcus neoformans H99 using confocal microscopy, histology, flow cytometry, and quantification of brain cytokine/chemokines and fungal burdens. C. neoformans was present in the perivascular space (PVS) of post-capillary venules. This was associated with a massive influx of blood-derived monocytes, neutrophils, and T lymphocytes into the PVS and a predominantly proinflammatory cytokine/chemokine response. Phagocytes containing cryptococci were present only in the lumen and corresponding PVS of post-capillary venules. Free cryptococci were observed breaching the glia limitans, the protective barrier between the PVS and the cerebral parenchyma. Parenchymal cryptococcomas were typically in direct contact with post-capillary venules and lacked surrounding immune cell infiltrates. Phagocyte depletion abrogated cryptococcoma formation and PVS infiltrates. Together, these observations suggest that cryptococcomas can originate via phagocyte-dependent transport across post-capillary venular endothelium into the PVS and thence via passage of free cryptococci into the brain. In conclusion, we demonstrate for the first time that the PVS of cortical post-capillary venules is the major site of the early innate immune response to, and phagocyte-dependent entry of, C. neoformans.
固有免疫系统是抵御隐球菌感染的主要防线,但它却促进了隐球菌感染中枢神经系统。我们对正常、嵌合、绿色荧光蛋白吞噬细胞阳性小鼠和吞噬细胞耗竭小鼠进行了详细的纵向神经隐球菌病研究,并使用共聚焦显微镜、组织学、流式细胞术以及脑细胞因子/趋化因子和真菌负荷的定量分析,研究了中枢神经系统固有免疫对新生隐球菌 H99 的反应。新生隐球菌存在于毛细血管后微静脉的血管周围腔隙(PVS)中。这与大量血液来源的单核细胞、中性粒细胞和 T 淋巴细胞涌入 PVS以及以促炎细胞因子/趋化因子反应为主有关。含有隐球菌的吞噬细胞仅存在于毛细血管后微静脉的管腔和相应的 PVS 中。游离隐球菌被观察到突破胶质界,这是 PVS 和大脑实质之间的保护性屏障。实质隐球菌瘤通常与毛细血管后微静脉直接接触,缺乏周围的免疫细胞浸润。吞噬细胞耗竭可消除隐球菌瘤的形成和 PVS 浸润。总之,这些观察结果表明,隐球菌瘤可以通过吞噬细胞依赖的方式穿过毛细血管后微静脉内皮细胞进入 PVS,然后通过游离隐球菌进入大脑而形成。总之,我们首次证明了皮质毛细血管后微静脉的 PVS 是固有免疫系统对新生隐球菌的早期反应和吞噬细胞依赖性进入的主要部位。