经济学人下载:癌症和微生物组 肠道里的元凶

Science and technology
科学技术

Cancer and the microbiome
癌症和微生物组

A punch in the gut
肠道里的元凶

How microbes promote liver cancer in the overweight
微生物如何诱发胖人的肝癌

OBESITY brings problems—notably heart disease, diabetes and cancer.
肥胖产生了问题─尤其是心脏病、糖尿病和癌症。

It is not hard to understand its connection with heart disease and diabetes: excess fat clogs arteries and messes around with the metabolism.
肥胖与心脏病、肥胖与糖尿病的联系不难理解：多余脂肪堵塞血管，使新陈代谢紊乱。

Its link with cancer is less intuitive.
但是肥胖与癌症的联系凭直觉就不能理解了。

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.
位于东京的日本癌症研究基金会的Shin Yoshimoto以及他的同事怀疑，这主要是因为研究人员的研究角度错误。

Most work in the field is focused on the cells of the human body.
此领域的多数工作只是集中在人身细胞的研究。

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认为，研究人员应当留心微生物组，这群生活在肠道的100万亿个细菌群。

Mostly, the microbiome is beneficial.
微生物组中的大多数都是有益的。

It helps with digestion and enables people to extract a lot more calories from their food than would otherwise be possible.
它们帮助消化，让人体从食物中分离出更多的能量。

Research over the past few years, however, has implicated it in diseases from atherosclerosis to asthma to autism.
然而，近几年的研究工作认为，微生物组是造成动脉硬化或孤独症等的病因。

Dr Yoshimoto and his colleagues would like to add liver cancer to that list.
但是，Yoshimoto以及他的同事则认为微生物组也是肝癌的病因。

Their paper making this accusation is published in this week'sNature, and it is a careful, step-by-step analysis of the matter.
他们的论文指出指控，发表在本周的《自然》杂志上。本篇文章进行了仔细、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.
文章开始便列举了事实，肥胖动物的肠道细菌与瘦的不同；某些细菌在新陈代谢过程中产生一种能引起炎症的分子；炎症诱发癌症。

They began their experiments by feeding laboratory mice a fatty diet, to make them obese.
他们通过实验小鼠进行实验，喂养高脂肪食物，让它们长胖。

Such mice, they found, are no more likely to develop cancer than those fed an abstemious diet.
他们发现，吃了脂肪含量高的小鼠患癌症的机率不高于饮食有度的小鼠。

Obesity alone, then, does not seem to cause tumours. But it might still promote them.
因此，单独肥胖一项因素不会引起肿瘤，但是仍然会诱发肿瘤。

Their next experiment therefore started by giving the mice a carcinogen known to trigger tumour formation throughout the body.
因此，他们下一步的实验就是喂养小鼠能在全身形成肿瘤的致癌物质。

One group was then fed standard fare while another got the high-fat diet.
一组实验小鼠喂养标准食物，另一组喂养高脂肪食物。

After 30 weeks, just 5% of the slim group had developed tumours, not in the liver but in the lungs.
30个星期后，体形瘦削的那组只有5%患有肿瘤，不是在肝脏，而是在肺部。

In the obese group, every animal had developed liver cancer.
体形肥胖的那组，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，研究人员先从肿瘤入手，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，他们发现，实验小鼠中癌化的肝脏细胞周围的细胞出现了老龄化的症状。

Such cells also emit chemical signals which promote inflammation, and thus encourage tumours.
这些老化细胞会释放出引发炎症的化学信号，并进一步诱发肿瘤。

The researchers suspected that these cells were being made senescent by something produced by gut bacteria.
研究人员怀疑，细胞出现老化是由肠道细菌产生的某些物质所致。

That suspicion was confirmed when they served some of their mice a cocktail of four antibiotics, to prune the animals' microbiomes.
研究人员混合了四种抗生素，喂养小鼠时，减少小鼠体内的微生物群。

This treatment lowered the number of senescent and cancerous cells, suggesting the microbes were indeed to blame for promoting cancer.
此时，他们的怀疑得到了证实。这种喂养方法减少了老化和癌化细胞的数量，表明微生物确实是诱发癌症的因素。

Dr Yoshimoto and his team then started to focus on which bacteria were causing the problem.
接下来，Yoshimoto和他和团队开始研究是何种微生物导致问题。

First, they discovered they could get the same cancer-suppressing effect using just vancomycin, an antibiotic that kills only “Gram-positive” bacteria.
首先，他们发现，用专杀“革兰氏阳性”细菌的抗生素万古霉素进行实验，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.
同时，他们发现，高脂肪饮食会提升化学物质脱氧胆酸的水平，万古霉素会使其降低。

Previous research had demonstrated too that DCA damages DNA in a way that promotes senescence.
先前的研究也发现，DCA会以一种诱发衰老的方式破坏DNA。

Dr Yoshimoto showed that lowering DCA levels in mice did indeed reduce the development of liver cancer.
Yoshimoto让人们看到，降低实验小鼠体内DCA的水平确实会减少诱发肝癌的机率。

Certain types of gut bacteria, including strains of Clostridium, are known to burp out DCA.
某些肠道细菌，包括梭状芽胞杆菌菌株，研究人员进行进一步的工作，包括研究小鼠粪便。

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.
他们研究发现，肥胖的小鼠粪便中OUT-1105这种梭状芽胞杆菌的水平要高于瘦削小鼠。

This strain, Dr Yoshimoto thinks, is the most likely culprit.
Yoshimoto认为，这种梭菌很有可能就是罪魁祸首。

There is, then, a chain of causation leading from the gut to the liver that promotes tumours in obese mice.
之后，他们又发现了一连串的因果现象，说明了肥胖小鼠体内从大肠到肝脏诱发肿瘤的成因。

And the chances are good that something similar pertains in Homo sapiens.
这提供了好机会，因为这个过程与人体内的过程相似，

Humans are not mice, of course.
虽然人不是老鼠，

But the two species' microbiomes often do behave in the same way.
但两者的运行机制还是相似的。

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.
人体内的微生物组令人烦恼，因为它会导致一些问题，而且由它导致的问题还在不断增加。假如由它导致的癌症防止不了，那么这就会刺激研究对微生物组进行调整，地防止产生疾病。

It will also, once again, emphasise the microbiome's role, for both good and ill, as an adjunct part of the human body
在此需要再一次地强调微生物组的作用，不论好与坏，毕竟它们都是人体的附属部分