Nanoparticulate matter exposure results in neuroinflammatory changes in the corpus callosum

Abstract

Epidemiological studies have established an association between air pollution particulate matter exposure (PM2.5) and neurocognitive decline. Experimental data suggest that microglia play an essential role in air pollution PM-induced neuroinflammation and oxidative stress. This study examined the effect of nano-sized particulate matter (nPM) on complement C5 deposition and microglial activation in the corpus callosum of mice (C57BL/6J males). nPM was collected in an urban Los Angeles region impacted by traffic emissions. Mice were exposed to 10 weeks of re-aerosolized nPM or filtered air for a cumulative 150 hours. nPM-exposed mice exhibited reactive microglia and 2-fold increased local deposition of complement C5/ C5α proteins and complement component C5a receptor 1 (CD88) in the corpus callosum. However, serum C5 levels did not differ between nPM and filtered air cohorts. These findings demonstrate white matter C5 deposition and microglial activation secondary to nPM exposure. The C5 upregulation appears to be localized to the brain.

Mixed Amphiphilic Polymeric Nanoparticles of Chitosan, Poly(vinyl alcohol) and Poly(methyl methacrylate) for Intranasal Drug Delivery: A Preliminary In Vivo Study

“…After i.n. administration, particles are expected to enter the CNS through the olfactory region and accumulate in the nose, the nose-to-brain tract (e.g., olfactory bulb) and the “bottom” brain ( Figure 3 a), before they disseminate to all the brain [ 21 , 55 ].…”

“…The existence of a nose-to-brain pathway that bypasses the BBB has been evidenced by the accumulation and harm caused by environmental nanoparticulate matter in the CNS [ 18 , 19 , 20 , 21 ]. With the emergence of nanomedicine, different types of pure drug nanocrystals and nanoparticles were designed and their CNS bioavailability following intranasal (i.n.)…”

Predisposition to Alzheimer’s and Age-Related Brain Pathologies by PM2.5 Exposure: Perspective on the Roles of Oxidative Stress and TRPM2 Channel

“…PM0.2-induced reduction in neurite growth was prevented by siRNA-mediated knockdown of the TNF-α expression, indicating that PM0.2-induced TNF-α generation by glial cells mediates such neurotoxicity (Cheng et al, 2016). Another recent study using 15/16-week-old mice shows that exposure to traffic-derived nPM (330 µg/m 3 , 5 h per day, and 3 days per week) for 10 weeks induced microglial cell activation and increased the deposition of complement C5/C5α proteins and C5a receptor 1 in the corpus callosum (Babadjouni et al, 2018). Taken together, these studies support that PM2.5 exposure causes AD-and age-related brain pathologies via inducing neuroinflammation (Figure 1).…”

A Review Ba(OH)2 : Transpor Ionik pada Barium Hidroksida di dalam Air dengan Konsep Termodinamika

“…Barium hidroksida adalah senyawa kimia dengan rumus kimia Ba (OH)2, yang mempunyai bentuk kristal putih (52)(53)(54)(55)(56)(57)(58)(59)(60)(61) Barium hidroksida ini memiliki sifat fisika (62)(63)(64)(65)(66)(67) dan sifat kimia seperti terlihat pada tabel di bawah ini. Barium merupakan suatu unsur kimia dalam tabel periodik yang memiliki lambang Ba dan nomor atom 56.Barium tidak ditemukan dialam dalam keadaan unsur bebas karena reaktivitas kimianya yang tinggi.Barium (68) secara kimiawi mirip dengan magnesium, kalsiumdan stronsium, namun lebih reaktif.…”