Cellular pathophysiology of sepsis associated encephalopathy (SAE) remains poorly characterised. Brain pathology in SAE, which is manifested by impaired perception, consciousness and cognition, results from multifactorial events, including high levels of systemic cytokines, microbial components and endotoxins, which all damage the brain barriers, instigate neuroinflammation and cause homeostatic failure. Astrocytes, being the principal homeostatic cells of the central nervous system contribute to the brain defence against infection. Forming multifunctional anatomical barriers, astroglial cells maintain brain-systemic interfaces and restrict the damage to the nervous tissue. Astrocytes detect, produce and integrate inflammatory signals between immune cells and cells of brain parenchyma, thus regulating brain immune response. In SAE astrocytes are present in both reactive and astrogliopathic states; balance between these states define evolution of pathology and neurological outcomes. In humans pathophysiology of SAE is complicated by frequent presence of comorbidities, as well as age-related remodelling of the brain tissue with senescence of astroglia; these confounding factors further impact upon SAE progression and neurological deficits.

脓毒症相关性脑病（SAE）的细胞病理生理学特征仍然很差。SAE的脑部病理表现为知觉，意识和认知受损，是多因素事件导致的，包括高水平的全身细胞因子，微生物成分和内毒素，这些都破坏了脑屏障，引起神经炎症并导致体内稳态失败。星形胶质细胞是中枢神经系统的主要稳态细胞，有助于大脑防御感染。星形胶质细胞形成多功能的解剖屏障，维持大脑系统界面并限制对神经组织的损害。星状细胞检测，产生并整合免疫细胞和脑实质细胞之间的炎症信号，从而调节大脑的免疫反应。在SAE中，星形胶质细胞以反应性和星形胶质变态存在。这些状态之间的平衡决定了病理学和神经学结局的演变。在人类中，SAE的病理生理学因合并症的频繁出现以及伴有星形胶质细胞衰老的大脑组织的年龄相关性重塑而变得复杂。这些混杂因素进一步影响了SAE进展和神经功能缺损。