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Science and technology
科學技術
Cancer and the microbiome
癌癥和微生物組
A punch in the gut
腸道里的元兇
How microbes promote liver cancer in the overweight
微生物如何誘發胖人的肝癌
OBESITY brings problems—notably heart disease, diabetes and cancer.
肥胖產生了問題―尤其是心臟病、糖尿病和癌癥。
It is not hard to understand its connection with heart disease and diabetes: excess fat clogs arteries and messes around with the metabolism.
肥胖與心臟病、肥胖與糖尿病的聯系不難理解：多余脂肪堵塞血管，使新陳代謝紊亂。
Its link with cancer is less intuitive.
但是肥胖與癌癥的聯系憑直覺就不能理解了。
Shin Yoshimoto of the Japanese Foundation for Cancer Research, in Tokyo, and his colleagues suspect this is at least partly because researchers have been looking for that link in the wrong place.
位于東京的日本癌癥研究基金會的Shin Yoshimoto以及他的同事懷疑，這主要是因為研究人員的研究角度錯誤。
Most work in the field is focused on the cells of the human body.
此領域的多數工作只是集中在人身細胞的研究。
But researchers should, Dr Yoshimoto believes, be at least as interested in the cells of the microbiome, the collection of 100 trillion bacteria that live in the gut.
Shin Yoshimoto認為，研究人員應當留心微生物組，這群生活在腸道的100萬億個細菌群。
Mostly, the microbiome is beneficial.
微生物組中的大多數都是有益的。
It helps with digestion and enables people to extract a lot more calories from their food than would otherwise be possible.
它們幫助消化，讓人體從食物中分離出更多的能量。
Research over the past few years, however, has implicated it in diseases from atherosclerosis to asthma to autism.
然而，近幾年的研究工作認為，微生物組是造成動脈硬化或孤獨癥等的病因。
Dr Yoshimoto and his colleagues would like to add liver cancer to that list.
但是，Yoshimoto以及他的同事則認為微生物組也是肝癌的病因。
Their paper making this accusation is published in this week'sNature, and it is a careful, step-by-step analysis of the matter.
他們的論文指出指控，發表在本周的《自然》雜志上。本篇文章進行了仔細、逐步的分析。
They start from the facts that fat animals have different gut bacteria from thin ones; that some bacteria produce inflammatory molecules as part of their metabolism; and that inflammation promotes cancer.
文章開始便列舉了事實，肥胖動物的腸道細菌與瘦的不同；某些細菌在新陳代謝過程中產生一種能引起炎癥的分子；炎癥誘發癌癥。
They began their experiments by feeding laboratory mice a fatty diet, to make them obese.
他們通過實驗小鼠進行實驗，喂養高脂肪食物，讓它們長胖。
Such mice, they found, are no more likely to develop cancer than those fed an abstemious diet.
他們發現，吃了脂肪含量高的小鼠患癌癥的機率不高于飲食有度的小鼠。
Obesity alone, then, does not seem to cause tumours. But it might still promote them.
因此，單獨肥胖一項因素不會引起腫瘤，但是仍然會誘發腫瘤。
Their next experiment therefore started by giving the mice a carcinogen known to trigger tumour formation throughout the body.
因此，他們下一步的實驗就是喂養小鼠能在全身形成腫瘤的致癌物質。
One group was then fed standard fare while another got the high-fat diet.
一組實驗小鼠喂養標準食物，另一組喂養高脂肪食物。
After 30 weeks, just 5% of the slim group had developed tumours, not in the liver but in the lungs.
30個星期后，體形瘦削的那組只有5%患有腫瘤，不是在肝臟，而是在肺部。
In the obese group, every animal had developed liver cancer.
體形肥胖的那組，每只小鼠都患上了肝癌。
To understand how this happened, the researchers began with the tumours and worked backwards.
要了解其中的原因，研究人員先從腫瘤入手，采用了反正法。
First, they found that the cancerous liver cells in their mice were generally accompanied by cells that had the symptoms of old age.
首先，他們發現，實驗小鼠中癌化的肝臟細胞周圍的細胞出現了老齡化的癥狀。
Such cells also emit chemical signals which promote inflammation, and thus encourage tumours.
這些老化細胞會釋放出引發炎癥的化學信號，并進一步誘發腫瘤。
The researchers suspected that these cells were being made senescent by something produced by gut bacteria.
研究人員懷疑，細胞出現老化是由腸道細菌產生的某些物質所致。
That suspicion was confirmed when they served some of their mice a cocktail of four antibiotics, to prune the animals' microbiomes.
研究人員混合了四種抗生素，喂養小鼠時，減少小鼠體內的微生物群。
This treatment lowered the number of senescent and cancerous cells, suggesting the microbes were indeed to blame for promoting cancer.
此時，他們的懷疑得到了證實。這種喂養方法減少了老化和癌化細胞的數量，表明微生物確實是誘發癌癥的因素。
Dr Yoshimoto and his team then started to focus on which bacteria were causing the problem.
接下來，Yoshimoto和他和團隊開始研究是何種微生物導致問題。
First, they discovered they could get the same cancer-suppressing effect using just vancomycin, an antibiotic that kills only “Gram-positive” bacteria.
首先，他們發現，用專殺“革蘭氏陽性”細菌的抗生素萬古霉素進行實驗，也能取得相同的抑癌效果。
They also observed, as prior research had suggested, that a fatty diet raised levels of a chemical called deoxycholic acid and that antibiotics lowered it.
同時，他們發現，高脂肪飲食會提升化學物質脫氧膽酸的水平，萬古霉素會使其降低。
Previous research had demonstrated too that DCA damages DNA in a way that promotes senescence.
先前的研究也發現，DCA會以一種誘發衰老的方式破壞DNA。
Dr Yoshimoto showed that lowering DCA levels in mice did indeed reduce the development of liver cancer.
Yoshimoto讓人們看到，降低實驗小鼠體內DCA的水平確實會減少誘發肝癌的機率。
Certain types of gut bacteria, including strains of Clostridium, are known to burp out DCA.
某些腸道細菌，包括梭狀芽胞桿菌菌株，研究人員進行進一步的工作，包括研究小鼠糞便。
And further detective work, including examination of the mice's faeces, revealed higher levels of a strain of Clostridium called OUT-1105 in the fat mice than in the thin ones.
他們研究發現，肥胖的小鼠糞便中OUT-1105這種梭狀芽胞桿菌的水平要高于瘦削小鼠。
This strain, Dr Yoshimoto thinks, is the most likely culprit.
Yoshimoto認為，這種梭菌很有可能就是罪魁禍首。
There is, then, a chain of causation leading from the gut to the liver that promotes tumours in obese mice.
之后，他們又發現了一連串的因果現象，說明了肥胖小鼠體內從大腸到肝臟誘發腫瘤的成因。
And the chances are good that something similar pertains in Homo sapiens.
這提供了好機會，因為這個過程與人體內的過程相似，
Humans are not mice, of course.
雖然人不是老鼠，
But the two species' microbiomes often do behave in the same way.
但兩者的運行機制還是相似的。
If cancer does end up being added to the growing list of problems which an upset microbiome can cause, that may stimulate research into ways of tweaking it to stop it causing disease.
人體內的微生物組令人煩惱，因為它會導致一些問題，而且由它導致的問題還在不斷增加。假如由它導致的癌癥防止不了，那么這就會刺激研究對微生物組進行調整，地防止產生疾病。
It will also, once again, emphasise the microbiome's role, for both good and ill, as an adjunct part of the human body
在此需要再一次地強調微生物組的作用，不論好與壞，畢竟它們都是人體的附屬部分
