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Description Introduction Recent studies suggest respiratory infections like SARS-CoV-2 can influence brain glial cell behavior. Early-life stress, such as neonatal stress, may predispose the nervous system to an exacerbated response during immune challenges. Thus, we investigated how early-life stress modifies glial cell activation and function during Sendai virus-induced lung inflammation, and assess its impact on neuroimmune responses and susceptibility to respiratory diseases in adulthood. Methods This study used a neonatal maternal separation (NMS) rat model in which Sprague Dawley rats were separated from their mother for 3 hours daily from postnatal days 3 to 12. At 8-10 weeks, rats were infected intranasally with Sendai virus, and brain glial cells were analyzed by flow cytometry post-infection. Results Activation markers of the microglia and astrocytes are modulated by Sendaï infection differently in response to stress and sex. Viral infection increased CD200 on astrocytes 4 days post-infection. At the same time, activated microglia MHCII levels were lower, with differences across sexes and between NMS and control groups. Conclusion Respiratory viral infections may affect glial cell activation, showing a pattern aligning with human SARS-CoV-2 observations. Early-life stress may further influence the glial response to such infections, emphasizing the role of developmental factors and immune challenges in shaping neuroimmune responses.
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Lauzon‐Joset et al. (2025) studied this question.
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