Ajmone-Cat MA, Spinello C, Valenti D, Franchi F, Macrì S, Vacca RA, Laviola G. Journal of Clinical Medicine. 2019; 8(10):1514. DOI: 10.3390/jcm8101514
- Adverse psychosocial experiences have been shown to modulate individual responses to immune challenges and affect mitochondrial functions.
- Results show chronic psychosocial stress altered the expression of neuroinflammatory markers in the hippocampal and hypothalamic regions, exacerbated the neuroinflammatory alterations induced by experimental GAS exposures in the same areas.
- Psychosocial stress exacerbated individual response to GAS administrations whereby mice exposed to both treatments exhibited altered cytokine and immune-related enzyme expression in the hippocampus and hypothalamus.
- Showed impaired mitochondrial respiratory chain complexes IV and V, and reduced adenosine triphosphate (ATP) production by mitochondria and ATP content.
- These brain abnormalities, observed in GAS-Stress mice, were associated with blunted titers of plasma corticosterone.
- Present data support the hypothesis that challenging environmental conditions, in terms of chronic psychosocial stress, may exacerbate the long-term consequences of exposure to GAS processes through the promotion of central immunomodulatory and oxidative stress.