自闭症竟然与它有关

在过去的几年里，越来越多的研究揭示了肠道微生物群对我们健康的重要性。它几乎可以影响一切，从我们对恐惧和消极刺激的反应，到我们的体重和精神健康，再到我们是否会患上像狼疮和1型糖尿病这样的自身免疫性疾病。

Now, a new study published in The Journal of Immunology has found a link between the gut microbiome and the neurodevelopmental condition autism using animal studies. However, it is not our own microbiome that affects whether or not we develop autism, the researchers say – it's our mom's.

现在，一项发表在《免疫学杂志》上的新研究发现了肠道微生物群和自闭症之间的联系。然而，研究人员表示，影响我们是否会患上自闭症的并不是我们自己的肠道微生物群，而是我们母亲的。

"The microbiome can shape the developing brain in multiple ways," John Lukens, lead researcher and PhD student from the University of Virginia School of Medicine, said in a statement."The microbiome is really important to the calibration of how the offspring's immune system is going to respond to an infection or injury or stress."As for autism, this link may come down to a particular molecule called interleukin-17a (or IL-17a), which is produced by the immune system. The molecule has already been associated with conditions like rheumatoid arthritis, multiple sclerosis, and psoriasis, and has been shown to serve an important role in preventing infections, notably those of the fungal kind. Importantly, it can also influence the way the brain develops in the womb.

来自弗吉尼亚大学医学院的首席研究员约翰·卢肯斯在一份声明中说道：“微生物群能够以多种方式塑造发育中的大脑。另外，微生物群对于校准后代的免疫系统来说也十分重要”。至于微生物群与自闭症的联系，这可能要归结到一种特殊的分子上——由免疫系统产生的白细胞介素17a。这种分子会导致人体患上类风湿性关节炎、多发性硬化症和牛皮癣，但又被证明在预防感染(尤其是真菌感染)方面发挥了重要作用。重要的是，它还可以影响大脑在子宫中发育的方式。

To test their hypothesis that autism may be triggered by the IL-17a molecule, the team blocked IL-17a in lab mice. The researchers recruited female mice from two separate laboratories – those from the first contained microflora in the gut that made them prone to an IL-17a-induced inflammatory response, whereas those from the second (the control) did not.

为了验证自闭症可能是由白细胞介素17a触发的假设，研究小组在实验室小鼠身上阻断了白细胞介素17a。研究人员从两个不同的实验室招募了两组雌性老鼠，第一个实验室的小鼠肠道内含有微生物群，这使它们更容易受到白细胞介素17a引起的炎症反应;而第二个实验室的小鼠则没有。

When the IL-17a molecule was artificially blocked (preventing IL-17a-induced inflammatory responses), the pups from both sets of mice were born with neuro-typical behaviors. Yet, when everything was left to progress without additional human intervention, the pups born from mothers in the first group went on to develop an autism-like neurodevelopmental condition, which affected social and repetitive behaviors.

当白细胞介素17a被人工阻断时，两组小鼠的幼崽出生时都有典型的神经行为。然而，当一切都在没有人为干预的情况下继续进行时，第一组的幼崽表现出了自闭症的行为。

To confirm that this was due to the group's unique microflora, the researchers performed a fecal transplant on mice from the second group using the feces of the mice from the first group. The idea here is to change the microflora of the second group so that it more closely resembles that of the first. And, as expected, the pups from the second group went on to develop an autism-like neurodevelopmental condition.

为了证实这确实是由于独特的微生物群导致的，研究人员使用第一组小鼠的粪便对第二组小鼠进行了粪便移植(这是为了改变第二组小鼠肠道内的微生物群，使其更接近于第一组的微生物群)。正如预期的那样，第二组小鼠所产下的幼崽也开始表现出自闭症的行为。

These are preliminary studies and may not translate to human pregnancies, but it does offer an interesting avenue to explore as far as autism research is concerned and provides strong evidence that the health of the mother's gut plays at least some role in the onset of neurodevelopmental conditions.

目前，这些还只是初步研究，可能对人类来说并不适用。但该研究确实提供了一个有趣的途径让我们来研究自闭症，它也提供了强有力的证据，证明母亲的肠道健康确实会影响后代的神经发育。