Mechanism of Microglial Cell Activation in the Benzophenone-3 Exposure Model

• Published in: Neuroscience Vol. 533; pp. 63 - 76
• Main Authors: Maciejska, Alicja, Pomierny, Bartosz, Krzyżanowska, Weronika, Starek-Świechowicz, Beata, Skórkowska, Alicja, Budziszewska, Bogusława
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 21.11.2023
• Subjects: benzophenone-3; cytokines; microglia activation; microglia polarization; primary microglia cells; CD; TNFα; IL; M1; NFκB; M2; microglia activation; BP-3; GR; benzophenone-3; IP-10; AP-1; LPS; microglia polarization; MFI; primary microglia cells; NLRP3; cytokines; SEM; TLR
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2023.10.002

•Benzophenone-3 disturbs the balance between subpopulations of microglial cells.•BP-3 reduces the level of the neuroprotective subpopulation of microglia cells.•BP-3 affects the activation of glucocorticoid receptors.•BP-3 increases the LPS-stimulated release of proinflammatory cytokines in vitro. Benzophenone-3 (BP-3) is the most commonly used UV filter in cosmetics, which is absorbed through the skin and crosses the blood–brain barrier. This compound increases extracellular glutamate concentrations, lipid peroxidation, the number of microglia cells and induces process of apoptosis. The aim of this study was to determine the effect of BP-3 on the activation and polarization of microglial cells in the frontal cortex and hippocampus of adult male rats exposed to BP-3 prenatally and then for two weeks in adulthood. It has been found, that exposure to BP-3 reduced the expression of the marker of the M2 phenotype of glial cells in both examined brain structures. An increase in the CD86/CD206 microglial phenotype ratio, expression of transcription factor NFκB and activity of caspase-1 were observed only in the frontal cortex, whereas BP-3 increased the level of glucocorticoid receptors in the hippocampus. The in vitro study conducted in the primary culture of rat frontal cortical microglia cells showed that BP-3 increased the LPS-stimulated release of pro-inflammatory cytokines IL-1α, IL-1β, TNFα, but in cultures without LPS there was decreased IL-1α, IL-6 and TNFα production, while the IL-18 and IP-10 was elevated. The obtained results indicate that differences in the level of immunoactivation between the frontal cortex and the hippocampus may result from the action of this compound on glucocorticoid receptors. In turn, changes in cytokine production in microglial cells indicate that BP-3 aggravates the LPS-induced immunoactivation.