小胶质细胞
外围设备
串扰
神经科学
炎症
星形胶质细胞
医学
中枢神经系统
免疫学
生物
内科学
物理
光学
作者
Maria Concetta Geloso,Luca Zupo,Valentina Corvino
标识
DOI:10.1016/j.neuint.2024.105872
摘要
A growing body of evidence supports the link between peripheral inflammation and impairment of neurologic functions, including mood and cognitive abilities. The pathogenic event connecting peripheral inflammation and brain dysfunction is represented by neuroinflammation, a pathogenic phenomenon that provides an important contribution to neurodegeneration and cognitive decline also in Alzheimer's, Parkinson's, Huntington's diseases, as well as in Multiple Sclerosis. It is driven by resident brain immune cells, microglia and astrocytes, that acquire an activated phenotype in response to proinflammatory molecules moving from the periphery to the brain parenchyma. Although a huge progress has been made in clarifying cellular and molecular mechanisms bridging peripheral and central inflammation, a clear picture has not been achieved so far. Therefore, experimental models are of crucial relevance to clarify knowledge gaps in this regard. Many findings demonstrate that systemic inflammation induced by pathogen-associated molecular patterns, such as lipopolysaccharide (LPS), is able to trigger neuroinflammation. Therefore, LPS-administration is widely considered a useful tool to study this phenomenon. On this basis, the present review will focus on in vivo studies based on acute and subacute effects of systemic administration of LPS, with special attention on the state of art of microglia and astrocyte response to peripheral challenge.
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