The Not Exactly Pocket Science experiment continues after the vast majority of people who commented liked the pilot post. I’m really enjoying this, for quite unexpected reasons. It’s forcing me to flex writing muscles that usually don’t get much of a workout. Writing short pieces means being far more economical with language and detail than usual. It means packing in as much information as possible while still keeping things readable. And it means blitz-reading papers and writing quickly without losing any accuracy.
One quick note before the good stuff: last time, a few people suggested that I put each NEPS item in a separate post, but the majority preferred multiple items per post. For now, I’m keeping it that way because otherwise, the longer pieces would be diluted by the smaller ones. We’ll see how that works for the foreseeable future.
Rising DAMPs – when enslaved bacteria turn our bodies against themselves
Our immune systems provide excellent defence against marauding hordes of bacteria, viruses and parasites, using sentinel proteins to detect the telltale molecules of intruders. But these defences can be our downfall if they recognise our own bodies as enemies.
All of our cells contain small energy-supplying structures called mitochondria. They’re descendents of ancient bacteria that were engulfed and domesticated by our ancestor cells. They’ve come a long way but they still retain enough of a bacterial flavour to confuse our immune system, should they break free of their cellular homes. An injury, for example, can set them free. If cells shatter, fragments of mitochondria are released into the bloodstream including their own DNA and amino acids that are typical of bacteria. Qin Zhang showed that trauma patients have far higher levels of such molecules in their blood than unharmed people. Our white blood cells have sentinel proteins that latch onto these molecules and their presence (incorrectly) says that a bacterial invasion is underway.
This discovery solves a medical mystery. People who suffer from severe injuries sometimes undergo a dramatic and potentially fatal reaction called “systemic inflammatory response syndrome” or SIRS, where inflammation courses through the whole body and organs start shutting down. This looks a lot like sepsis, an equally dramatic response to an infection. However, crushing injuries and burns can cause SIRS without any accompanying infections. Now we know why – SIRS is caused by the freed fragments of former bacteria setting off a false alarm in the body. The technical term for these enemies within is “damage-associated molecular patterns” or DAMPs.
More from Heidi Ledford at Nature News
Reference: Nature DOI:10.1038/nature08780
Different gut bacteria lead to mice to overeat
On Wednesday, I wrote about the hidden legions residing up your bum – bacteria and other microbes, living in their millions and outnumbering your cells by ten to one. These communities wield a big influence over our health, depending on who their members are. Matam Vijay-Kumar found that different species colonise the guts of mice with weakened immune systems, and this shifted membership is linked to metabolic syndrome, a group of obesity-related symptoms that increase the risk of heart disease and type 2 diabetes.
Vijay-Kumar’s mice lacked the vital immune gene TLR5, which defends the gut against infections. Their bowels had 116 species of bacteria that were either far more or less common than usual. They also overate, became fat, developed high blood pressure and became resistant to insulin – classic signs of metabolic syndrome. When Vijay-Kumar transplanted the gut menagerie from the mutant mice to normal ones, whose own bacteria had been massacred with antibiotics, the recipients also developed signs of metabolic syndrome. It was clear evidence that the bacteria were causing the symptoms and not the other way round.
Vijay-Kumar thinks that without the influence of TLR5, the mice don’t know what to make of their unusual gut residents. They react by releasing chemicals that trigger a mild but persistent inflammation. These same signals encourage the mice to eat more, and they make local cells resistant to the effects of insulin. Other aspects of the metabolic syndrome soon follow. The details still need to be confirmed but for now, studies like this show us how foolish it is to regard obesity as a simple matter of failing willpower. It might all come down to overeating and inactivity, but there are many subtle reasons why an individual might eat too much. The microscopic community within our guts are one of them.
Reference: Science DOI:10.1126/science.1179721
The stretchy iron-clad beards of mussels
For humans, beards are for catching food, looking like a druid, and getting tenure. But other animals have beards with far more practical purposes – mussels literally have beards of iron that they use as anchors. The beard, or byssus, is a collection of 50-100 sticky threads. Each is no thicker than a human hair but they’re so good at fastening the mussels to wave-swept rocks that scientists are using them as the inspiration for glue. So they should. The byssus is a marvel of bioengineering – hard enough to hold the mussel in place, but also stretchy enough so that they can extend without breaking.
The mussel secretes each thread with its foot, first laying down a protein-based core and then covering it in a thick protective layer that’s much harder. When Matthew Harrington looked at the strands under a microscope, he saw that the outer layer is a composite structure of tiny granules amid a looser matrix. The granules consist of iron and a protein called mfp-1, heavily linked to one other – this makes the byssus hard. The matrix is a looser collection of the same material, where mfp-is 1 heavily coiled but easy to straighten – this lets the byssus stretch. The granules have a bit of give to them but at higher strains, they hold firm while the matrix continues extending. If cracks start to form, the granules stop them from spreading.
It’s unclear how the mussel creates such a complicated pattern, but Harrington suggests that it could be deceptively simple – changing a single amino acid in the mfp-1 protein allows it to cross-link more heavily with iron. That’s the difference between the tighter granular bundles, and the looser ones they sit among.
Reference: Science DOI:10.1126/science.1181044
Cause of dinosaur extinction
Sixty-five million years ago, the vast majority of dinosaurs were wiped out. Now, a new paper reveals the true cause of their demise – legions of zombies armed with chaingu… wait… oh. Right. An asteroid. You knew that.
More from Mark Henderson at the Times
Reference: Science DOI:10.1126/science.1177265
You are outnumbered by a factor of 10 to one, by forces you cannot see. Your body has around ten trillion cells, but it’s also home to a hundred trillion bacteria. For every gene in your genome, there are 100 bacterial ones. Most of these are found the dark, dank environment of your bowel but their incredible diversity is being brought to the surface. Say hello to the gut metagenome.
Together with a team of international scientists, Junjie Qin and Ruiqiang Li from BGI-Shenzen had the unenviable task of studying the bacteria from the faeces of 124 Europeans. They used a formidable and audacious technique called metagenomics, which analyses all the genetic material in a sample, without bothering to culture the individual species first. It’s a shoot-first-ask-questions-later method that captures all the data and lets other programmes sort out the mess.
Stool samples from 33 people have already been analysed in this way, but Qin and Li managed to sequence almost 200 times as much DNA. Brace yourself for some big numbers. Their project uncovered just under 3.3 million bacterial genes, more than 150 times as many as reside in the entire human genome. By their estimate, your bowel and mine harbour at least 160 bacterial species each and we share many of our tenants (I say bacteria, but around 1% of the genes came from archaea, a superficially similar group but one that’s actually as different from bacteria as bacteria are from us).
The quest to understand gut microbes may seem like an arcane niche of science, but it’s actually very important for public health. We rely on these microscopic passengers more than we realise. They harvest energy from our food, provide us with nutrients that would otherwise be denied to us, prevent the growth of harmful bacteria, and more. In many ways, they’re like a forgotten organ. They can also go rogue, changing their community in ways that are linked to obesity or bowel diseases. Indeed, Qin and Li showed that the gut microbiome of a health person looks very different to that of someone with a bowel condition like Crohn’s disease or ulcerative colitis.
All in all, over 1,000 species make their living in the human bowel but a common cadre of 57 are shared by the vast majority of us. Even for this common set, each individual species could be thousands of times more common in your gut compared to mine. With such variation, it’s no wonder that earlier smaller studies concluded that people have very different gut lodgers.
You are not alone. Even if you’re currently reading this in complete isolation, you are still far from a singular individual. You’re more of a colony – one human, together with microbes in their trillions. For every one of your own genes, your body is also host to thousands of bacterial ones. Some of the most important of these tenants – the microbiota – live in our gut. Their genes, collectively known as our microbiome, provide us with the ability to break down sources of food, like complex carbohydrates, that we would otherwise find completely indigestible.
Peter Turnbaugh from the Washington University School of Medicine has spent his career studying the microbiome. His latest work reveals both tremendous differences and similarities between the bacterial tenants of our digestive systems. Your bowels may be home to very different species of bacteria to mine, but both our sets share a core group of genes.
Turnbaugh likens the situation within our guts to that of islands. Real islands may be home to very different species of animals but all have representatives that perform certain roles; there will always be grazers, predators, insect-eating specialists, fishermen and so on. Across islands, animals approach a set of core lifestyles in different ways, and so it is with the microbiota – every man is an island, home to unique collections of bacteria that nonetheless carry out some core functions. And the further an person’s microbiota strays from this standard template, the more likely they are to be obese.