Olfactory bulb microglia activation mediated neuronal death in real-ambient particulate matter exposure mice with depression-like behaviors

Particulate matter and Alzheimer’s disease: an intimate connection

“…Transmission electron microscopy revealed particles accumulated in the olfactory bulbs of PM 2.5 -exposed animals [38]. Interestingly, several findings from this study, including the increased inflammatory response, were highest after 4 weeks, indicating a compensatory response or tolerance may have been achieved by 8 weeks of PM 2.5 exposure [38]. Within the olfactory bulbs of PM 2.5 -exposed animals, significantly heightened p-tau levels have been found compared with FA-exposed counterparts [31].…”

“…After PM is inhaled through the nose, it translocates from the olfactory nerve to the olfactory bulb. Continuously exposing C57BL/6 mice to PM 2.5 (mean daily 140.18 μg/m 3 ) for 4 or 8 weeks induced changes in the olfactory bulbs, including neuronal apoptosis, cell disorganization, and increased TNF-α signaling [38]. Transmission electron microscopy revealed particles accumulated in the olfactory bulbs of PM 2.5 -exposed animals [38].…”

“…Continuously exposing C57BL/6 mice to PM 2.5 (mean daily 140.18 μg/m 3 ) for 4 or 8 weeks induced changes in the olfactory bulbs, including neuronal apoptosis, cell disorganization, and increased TNF-α signaling [38]. Transmission electron microscopy revealed particles accumulated in the olfactory bulbs of PM 2.5 -exposed animals [38]. Interestingly, several findings from this study, including the increased inflammatory response, were highest after 4 weeks, indicating a compensatory response or tolerance may have been achieved by 8 weeks of PM 2.5 exposure [38].…”

“…Further investigation into the microglial response demonstrated an M1 phenotype as evidenced by enhanced CD11b and CD86 coupled with increased IL-6 and IL-8 by PM 2.5 exposure [18,46]. Another study treated BV2 cells, a microglial cell line, with 100 μg/ml PM 2.5 for 12 h and neuroblastoma N2A cells with a conditioned medium from the BV2 cells for 24 h [38]. PM 2.5 -treated BV2 cells exhibited significantly increased TNF-α levels, pointing to direct activation of microglia cells by PM 2.5 [38].…”

“…Another study treated BV2 cells, a microglial cell line, with 100 μg/ml PM 2.5 for 12 h and neuroblastoma N2A cells with a conditioned medium from the BV2 cells for 24 h [38]. PM 2.5 -treated BV2 cells exhibited significantly increased TNF-α levels, pointing to direct activation of microglia cells by PM 2.5 [38]. The coculture system resulted in apoptosis among N2A cells, indicating PM 2.5 could cause neuronal cell death by inducing systemic inflammation and its associated downstream effects (microglia activation, TNF-α release) or via direct action [38].…”