4.5 Review

Microbial Induction of Vascular Pathology in the CNS

期刊

JOURNAL OF NEUROIMMUNE PHARMACOLOGY
卷 5, 期 3, 页码 370-386

出版社

SPRINGER
DOI: 10.1007/s11481-010-9208-9

关键词

LCMV; brain; vasculature; blood vessel; blood brain barrier; malaria; Theiler's virus; Ebola virus; Lassa fever virus; Dengue virus; hemorrhagic fevers; ventricles; cerebral spinal fluid; neutrophils; monocytes; T cells

资金

  1. National Institutes of Health
  2. National Research Service Award [NS061447-01]
  3. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [ZIANS003112, F32NS061447] Funding Source: NIH RePORTER

向作者/读者索取更多资源

The central nervous system (CNS) is a finely tuned organ that participates in nearly every aspect of our day-to-day function. Neurons lie at the core of this functional unit and maintain an active dialogue with one another as well as their fellow CNS residents (e.g. astrocytes, oligodendrocytes, microglia). Because of this complex dialogue, it is essential that the CNS milieu be tightly regulated in order to permit uninterrupted and efficient neural chemistry. This is accomplished in part by anatomical barriers that segregate vascular components from the cerebral spinal fluid (CSF) and brain parenchyma. These barriers impede entry of noxious materials and enable the CNS to maintain requisite protein and ionic balances for constant electrochemical signaling. Under homeostatic conditions, the CNS is protected by the presence of specialized endothelium/epithelium, the blood brain barrier (BBB), and the blood-CSF barrier. However, following CNS infection these protective barriers can be comprised, sometimes resulting in severe neurological complications triggered by an imbalance or blockage of neural chemistry. In some instances, these disruptions are severe enough to be fatal. This review focuses on a selection of microbes (both viruses and parasites) that compromise vascular barriers and induce neurological complications upon gaining access to the CNS. Emphasis is placed on CNS diseases that result from a pathogenic interplay between host immune defenses and the invading microbe.

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