Abstract
The embryonic stage is the most vulnerable period for congenital abnormalities. Due to its prolonged developmental course, the central nervous system (CNS) is susceptible to numerous genetic, epigenetic, and environmental influences. During embryo implantation, the CNS is more vulnerable to external influences such as environmental tobacco smoke (ETS), increasing the risk for delayed fetal growth, sudden infant death syndrome, and immune system abnormalities. This study aimed to evaluate the effects of in utero exposure to ETS on neuroinflammation in the offspring of pregnant mice challenged or not with lipopolysaccharide (LPS). After the confirmation of mating by the presence of the vaginal plug until offspring birth, pregnant C57BL/6 mice were exposed to either 3R4F cigarettes smoke (Kentucky University) or compressed air, twice a day (1h each), for 21 days. Enhanced glial cell and mixed cell cultures were prepared from 3-day-old mouse pups. After cell maturation, both cells were stimulated with LPS or saline. To inhibit microglia activation, minocycline was added to the mixed cell culture media 24 h before LPS challenge. To verify the influence of in utero exposure to ETS on the development of neuroinflammatory events in adulthood, a different set of 8-week-old animals was submitted to the Autoimmune Experimental Encephalomyelitis (EAE) model. The results indicate that cells from LPS-challenged pups exposed to ETS in utero presented high levels of proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNFα) and decreased cell viability. Such a proinflammatory environment could modulate fetal programming by an increase in microglia and astrocytes miRNA155. This scenario may lead to the more severe EAE observed in pups exposed to ETS in utero.
Highlights
Over the course of the 20th century, more than 100 million people died from smoking, and this number is expected to reach one billion in the 21st century (World Health Organization, 2017)
The group exposed to environmental tobacco smoke (ETS) and challenged with LPS had increased astrocytes levels compared to Control Group (CO) (p < 0.0001), ETS (p < 0.01), and LPS (p < 0.0001) (Figure 2A)
After verifying an increased inflammatory response by glial cells in ETS-exposed groups challenged with LPS, we investigated whether this inflammation process could change cellular viability in a mixed cell culture composed of 3% microglia cells, 39% astrocytes, and 58% neurons (Supplementary Figure S3)
Summary
Over the course of the 20th century, more than 100 million people died from smoking, and this number is expected to reach one billion in the 21st century (World Health Organization, 2017) Countries such as Brazil, the United Kingdom, and Australia managed to reduce the numbers of smokers through the implementation of public policies, maternal smoking and passive smoking during pregnancy are still important public health concerns. From mainstream smoke – the one exhaled by the smoker, – sidestream smoke streams from the burning tip of the cigarette, passing through no type of filter (cigarette or lung) and being more harmful than mainstream smoke It is formed by incomplete combustion, including greater amounts of toxic and carcinogenic substances per unit of mass (Mello et al, 2001; Organização Pan-Americana da Saúde, 2008; Salmória and Oliveira, 2008)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
