自閉癥竟然與它有關(guān)

在過去的幾年里，越來越多的研究揭示了腸道微生物群對我們健康的重要性。它幾乎可以影響一切，從我們對恐懼和消極刺激的反應，到我們的體重和精神健康，再到我們是否會患上像狼瘡和1型糖尿病這樣的自身免疫性疾病。

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.

現(xiàn)在，一項發(fā)表在《免疫學雜志》上的新研究發(fā)現(xiàn)了腸道微生物群和自閉癥之間的聯(lián)系。然而，研究人員表示，影響我們是否會患上自閉癥的并不是我們自己的腸道微生物群，而是我們母親的。

"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.

來自弗吉尼亞大學醫(yī)學院的首席研究員約翰·盧肯斯在一份聲明中說道：“微生物群能夠以多種方式塑造發(fā)育中的大腦。另外，微生物群對于校準后代的免疫系統(tǒng)來說也十分重要”。至于微生物群與自閉癥的聯(lián)系，這可能要歸結(jié)到一種特殊的分子上——由免疫系統(tǒng)產(chǎn)生的白細胞介素17a。這種分子會導致人體患上類風濕性關(guān)節(jié)炎、多發(fā)性硬化癥和牛皮癬，但又被證明在預防感染(尤其是真菌感染)方面發(fā)揮了重要作用。重要的是，它還可以影響大腦在子宮中發(fā)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.

為了驗證自閉癥可能是由白細胞介素17a觸發(fā)的假設，研究小組在實驗室小鼠身上阻斷了白細胞介素17a。研究人員從兩個不同的實驗室招募了兩組雌性老鼠，第一個實驗室的小鼠腸道內(nèi)含有微生物群，這使它們更容易受到白細胞介素17a引起的炎癥反應;而第二個實驗室的小鼠則沒有。

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.

當白細胞介素17a被人工阻斷時，兩組小鼠的幼崽出生時都有典型的神經(jīng)行為。然而，當一切都在沒有人為干預的情況下繼續(xù)進行時，第一組的幼崽表現(xiàn)出了自閉癥的行為。

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.

為了證實這確實是由于獨特的微生物群導致的，研究人員使用第一組小鼠的糞便對第二組小鼠進行了糞便移植(這是為了改變第二組小鼠腸道內(nèi)的微生物群，使其更接近于第一組的微生物群)。正如預期的那樣，第二組小鼠所產(chǎn)下的幼崽也開始表現(xiàn)出自閉癥的行為。

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，這些還只是初步研究，可能對人類來說并不適用。但該研究確實提供了一個有趣的途徑讓我們來研究自閉癥，它也提供了強有力的證據(jù)，證明母親的腸道健康確實會影響后代的神經(jīng)發(fā)育。