Prenatal air pollution exposure induces neuroinflammation and predisposes offspring to weight gain in adulthood in a sex‐specific manner

Bolton, Jessica L.; Smith, Susan; Huff, Nicole; Gilmour, M. Ian; Foster, W. Michael; Auten, Richard L.; Bilbo, Staci D.

doi:10.1096/fj.12-210989

Cited by 205 publications

(195 citation statements)

References 53 publications

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“…Besides that, we observed decreased plasma levels of glutathione and folate only in adult male [27], corroborating that female and male offspring responded differently to methyl donor deficiency in utero. Indeed, studies on epigenetic mechanisms have shown that males may be more susceptible in adulthood due to epigenetic marks generated during embryonic period [36,37]. The offspring's care, usually associated to females, is suggested as a selective pressure agent [38].…”

Section: Discussionmentioning

confidence: 99%

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Silva¹,

Fernandes²,

Agamme³

et al. 2017

Biol Med (Aligarh)

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Alzheimer's disease (AD) is characterized by progressive neurodegenerative impairment of the central nervous system and is the most prevalent form of dementia. Considering the influence of maternal nutrition on fetal programming, which consequences usually come later in life, we investigated whether maternal vitamin B deficiency during early development alters the offspring expression of genes related to AD etiopathogenesis. Mice dams were submitted to experimental diet one month before and during pregnancy or pregnancy/lactation and, after birth, their offspring were distributed into three groups: control "CT", deficient pregnancy "DP" and deficient pregnancy and lactation "DPL". At postnatal day (PND) 0, a significant decrease of App in females (p=0.007) and App and Bace1 in males (p=0.030 and p=0.040, respectively) was observed when compared to CT group. At PND 28, DPL female presented an increase of App, Bace1 and Ps1 gene expression when compared to CT (p=0.003, p=0.003 and p=0.002, respectively) and DP groups (p=0.017, p=0.005 and p=0.002, respectively). In males at PND 28, a decrease of App and Ps1 was observed in both DP (p=0.012; p=0.001) and DPL (p=0.001; p=0.04) when compared to CT group. No differences were observed in females and males at PND 210. Regarding APP, BACE1 and PS1 protein expression and global DNA methylation pattern, no difference was observed throughout development in female or male offspring. Regarding behavioral evaluations, no changes were observed in the object recognition task, but the DPL males presented lower locomotor activity when compared to DP (p=0.028) and CT (p=0.003) groups. In conclusion, the early exposition to vitamin B deficiency alters the expression of genes related to AD.

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Section: Discussionmentioning

confidence: 99%

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Silva¹,

Fernandes²,

Agamme³

et al. 2017

Biol Med (Aligarh)

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“…La dégradation de la qualité de l'alimentation dans les pays déve-loppé et la contamination de notre environnement par des perturbateurs endocriniens sont les facteurs les plus souvent incriminés pour comprendre l'épidémie actuelle d'obésité et de maladies métaboliques. Cependant, l'exposition chronique à la pollution atmosphérique pourrait aussi jouer un rôle, comme le suggère en particulier une étude chez la souris qui montre que l'exposition foetale à des gaz d'échappement diesel augmente la réponse post-natale à un régime obésogène, avec des effets qui varient selon le sexe de l'individu (Bolton et al 2012, Bolton et al 2013). …”

Section: Discussion Et Conclusionunclassified

“…Aux concentrations d'exposition les plus élevées, l'expression génique placentaire de plusieurs cytokines proinflammatoires (interleukines IL-4, IL-5, IL-6, IL-12a et b) est très largement augmentée (Fujimoto et al 2005). L'exposition in utero à des concentrations élevées de DE induit aussi une augmentation marquée de l'expression d'interleukines (IL-1b, IL-6, IL-10) et de chimiokines (chemokine ligand 2 et fractalkine) dans le cerveau des foetus à terme (Bolton et al 2012 (Valentino et al 2016).…”

Section: Exposition Par Inhalationunclassified

Exposition aux gaz d’échappement diesel durant la gestation : quelles conséquences sur le développement foeto-placentaire ? Apport des modèles animaux

Valentino¹,

Tarrade²,

Chavatte‐Palmer³

2016

bavf

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La pollution atmosphérique est un problème majeur pour la santé humaine, causant 3,7 millions de décès prématurés en 2012 dans le monde. Les personnes âgées, les enfants ou les asthmatiques sont les cibles des messages de prévention lors de pics de pollution alors que les femmes enceintes sont le plus souvent négligées. Pourtant, les études épidémiologiques et les travaux sur les modèles animaux indiquent que la pollution atmosphérique et ses composants peuvent perturber la fonction placentaire, réduire la croissance foetale et induire un stress oxydant et une inflammation. A long terme, ces effets peuvent participer à l'augmentation des risques de maladies métaboliques chez l'adulte. Il est donc important d'inclure les femmes enceintes dans les messages de prévention lors de pics de pollution atmosphérique et de continuer la recherche sur les effets à long terme grâce au recours aux modèles animaux.

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“…Epidemiologic studies evidence that diabetic individuals are adversely affected by air pollution exposure [9] Obesity is the primary cause underlying the development of insulin resistance and type 2 diabetes [10] and is associated with chronically elevated plasma levels of IL-6 [11]. Studies in experimental rat models have shown that air pollution agg ravates inflammation and insulin resistance especially in obese animals [12].…”

Section: Introductionmentioning

confidence: 99%

10.4172/2155-9880.1000255

Matsuda¹

2013

J Clin Exp Cardiolog

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Recent experimental data have provided associations between ambient PM 2.5 (fine particulate matter; diameter ≤ 2.5 µm) and propensity to inflammation and chronic diseases especially among susceptible groups, such as elderly people. There is cumulative evidence that type-2 diabetes mellitus is a chronic inflammatory state aggravated by factors that promote endothelium inflammation. Accordingly our hypothesis that the exposure of aged obese population to PM 2.5 might aggravate type-2 diabetes, we used a model of aged, diet-induced obese mice. C57BL6 male mice were fed with regular chow (n=30; RC) or high-fat chow (n=36; HF) during one-year and randomly assigned to filtered (FA-RC, n=16; FA-HF, n=19) or PM 2.5 concentrated air (600 µg.m -3 ) (EXP-RC, n=14; EXP-HF, n=17) chambers to have a daily 1 hour exposition during consecutive 30-days. Fast glycemia was measured before the animals were euthanized. The Institution's Ethics Committee approved all experimental procedures. Heart mRNA content of selected migration, signalization and adhesion proteins were measured by SYBR Green fluorescence Real Time RT-PCR protocol using appropriate primers. There were no difference between RC-EXP and RC-FA nor between HF-EXP and HF-FA body weight. Regarding fast glycemia, both, RC and HF groups, were diabetic, but only the HF group was affected by acute exposure to PM 2.5 (mean ± SD, EXP-HF vs FA-HF, 172.8 ± 23.4 vs 156.7 ± 17.6, p <0.05; EXP-RC vs FA-RC, 149.8 ± 19.2, 139.7 ± 15.3, ns; ANOVA). The gene expression profile of E-selectin, IL-6, VCAM-1, ICAM-1 and MMP-9, was differently affected by PM 2.5 in heart and lung. Proteins activated by inflammatory stimuli involved in the inhibition of insulin signaling are being investigated.

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Prenatal air pollution exposure induces neuroinflammation and predisposes offspring to weight gain in adulthood in a sex‐specific manner

Cited by 205 publications

References 53 publications

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Exposition aux gaz d’échappement diesel durant la gestation : quelles conséquences sur le développement foeto-placentaire ? Apport des modèles animaux

10.4172/2155-9880.1000255

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