CHRONIC SOCIAL STRESS ALTERS CHOROID PLEXUS HOMEOSTASIS AND NEUROIMMUNE INTERACTIONS

Chronic stress is known to alter blood brain barrier integrity and function, contributing to neuroinflammatory processes implicated in various neuropsychiatric disorders. Despite its crucial role in maintaining central nervous system (CNS) homeostasis and immune surveillance, the impact of chronic stress on the blood-cerebrospinal fluid (CSF) barrier, the choroid plexus (ChP), remains largely overlooked. Using two different mouse models, we investigate how chronic social defeat (CSD) stress and early life stress (ELS) alter ChP function, with a focus on immune cell populations, glucocorticoid receptor expression and barrier integrity.
Given the ChP’s role in trafficking immune cells into the CNS, we examined stress-induced changes in immune cell composition using fluorescence-activated cell sorting (FACS) and immunohistochemistry. First results show a significant increase in some dendritic cell and T cell populations following CSD, suggesting a potential role in stress-induced neuroimmune dysregulation. Current analyses aim to determine whether stress affects GR signaling and tight junction integrity, which may compromise ChP function and contribute to CNS pathology. Additionally, to explore how stress early in life influences ChP function later in life, we are assessing whether ELS leads to similar immune and barrier alterations.
These findings highlight the choroid plexus's emerging role in mediating neuroimmune responses to stress and emphasize the importance of further research to better understand stress-related psychiatric disorders.