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Phenotypic overlap between atopic dermatitis and autism

机译：特应性皮炎和自闭症之间的表型重叠

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Autism, a childhood behavioral disorder, belongs to a large suite of diseases, collectively referred to as autism spectrum disorders (ASD). Though multifactorial in etiology, approximately 10% of ASD are associated with atopic dermatitis (AD). Moreover, ASD prevalence increases further as AD severity worsens, though these disorders share no common causative mutations. We assessed here the link between these two disorders in the standard, valproic acid mouse model of ASD. In prior studies, there was no evidence of skin involvement, but we hypothesized that cutaneous involvement could be detected in experiments conducted in BALB/c mice. BALB/c is an albino, laboratory-bred strain of the house mouse and is among the most widely used inbred strains used in animal experimentation. We performed our studies in valproic acid (VPA)-treated BALB/c hairless mice, a standard mouse model of ASD. Mid-trimester pregnant mice received a single intraperitoneal injection of either valproic acid sodium salt dissolved in saline or saline alone on embryonic day 12.5 and were housed individually until postnatal day 21. Only the brain and epidermis appeared to be affected, while other tissues remain unchanged. At various postnatal time points, brain, skin and blood samples were obtained for histology and for quantitation of tissue sphingolipid content and cytokine levels. AD-like changes in ceramide content occurred by day one postpartum in both VPA-treated mouse skin and brain. The temporal co-emergence of AD and ASD, and the AD phenotype-dependent increase in ASD prevalence correlated with early appearance of cytokine markers (i.e., interleukin [IL]-4, 5, and 13), as well as mast cells in skin and brain. The high levels of interferon (IFN)γ not only in skin, but also in brain likely account for a significant decline in esterified very-long-chain N-acyl fatty acids in brain ceramides, again mimicking known IFNγ-induced changes in AD. Baseline involvement of both AD and ASD could reflect concurrent neuro- and epidermal toxicity, possibly because both epidermis and neural tissues originate from the embryonic neuroectoderm. These studies illuminate the shared susceptibility of the brain and epidermis to a known neurotoxin, suggesting that the atopic diathesis could be extended to include ASD.
机译：自闭症是一种儿童行为障碍，属于大量疾病，统称为自闭症谱系障碍（ASD）。虽然在病因中的多因素，但大约10％的ASD与特应性皮炎（AD）相关。此外，随着广告严重程度恶化，ASD患病率进一步增加，尽管这些疾病没有共同的致病性突变。我们在这里评估了这两种疾病之间的联系，标准的ASD的丙戊酸小鼠模型。在先前的研究中，没有皮肤受累的证据，但我们假设可以在Balb / C小鼠进行的实验中检测皮肤参与。 BALB / C是阿尔巴尼诺，实验室繁殖的房屋鼠标，是在动物实验中使用的最广泛使用的近铬菌株之一。我们在丙戊酸（VPA） - 治疗的Balb / C无毛或ASD的标准鼠标模型中进行了研究。妊娠中期的孕孕小鼠单独腹膜内注射羟丙基酸钠盐，单独溶解在盐水或盐水中的胚胎第12.5天，并单独饲养直至产后第21天。只有脑和表皮似乎受到影响，而其他组织保持不变。在各种后时间点，脑，皮肤和血液样品获得组织学和组织鞘脂含量和细胞因子水平的定量。在VPA治疗的小鼠皮肤和大脑中，Day Playum发生的锡酰胺含量的许可变化。 AD和ASD的时间共出，以及ASD患病率的ASD表型依赖性增加与细胞因子标记的早期外观相关（即白细胞介素[IL] -4,5和13），以及皮肤中的肥大细胞和大脑。高水平的干扰素（IFN）γ不仅在皮肤中，而且在脑中也可能占脑酰胺中酯化的非常长链N-酰基脂肪酸的显着下降，再次模仿已知的IFNγ诱导的AD变化。 AD和ASD的基线参与可以反映并发神经和表皮毒性，可能是因为表皮和神经组织源自胚胎神经外胚层。这些研究阐明了脑和表皮的共同敏感性，以众所周知的神经毒素，表明特应素质抑制可以扩展到包括ASD。

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