Abstract：
While brain swelling, associated with fluid accumulation, is a known feature of pediatric cerebral malaria (CM), how fluid and macromolecules are drained from the brain during recovery from CM is unknown. Using the experimental CM (ECM) model, we show that fluid accumulation in the brain during CM is driven by vasogenic edema and not by perivascular cerebrospinal fluid (CSF) influx. We identify that fluid and molecules are removed from the brain extremely quickly in mice with ECM to the deep cervical lymph nodes (dcLNs), predominantly through basal routes and across the cribriform plate and the nasal lymphatics. In agreement, we demonstrate that ligation of the afferent lymphatic vessels draining to the dcLNs significantly impairs fluid drainage from the brain and lowers anti-malarial drug recovery from the ECM syndrome. Collectively, our results provide insight into the pathways that coordinate recovery from CM.
摘要：
脑肿胀的同时,与液体积聚有关，是小儿脑型疟疾（CM）的已知特征，在从CM恢复过程中，液体和大分子是如何从大脑中排出的，目前尚不清楚。使用实验CM(ECM)模型，我们表明，CM期间大脑中的液体积聚是由血管源性水肿驱动的，而不是由血管周围脑脊液（CSF）流入驱动的。我们发现，在具有ECM的小鼠中，液体和分子极快地从大脑中去除到深颈部淋巴结（dcLN），主要通过基础途径，穿过筛板和鼻淋巴管。在协议中,我们证明,引流到dcLN的传入淋巴管结扎会显著损害脑液引流,并降低抗疟疾药物从ECM综合征的恢复.总的来说，我们的结果提供了对协调从CM恢复的途径的洞察。
