As I’ve noted before, our bodies are riddled with microbes – there are more of them than there are of us (if you go by shear number). But where do they come from? Each individual has a complex ecosystem of commensal (harmless) microbes that live on our skin, in our nose, mouth, ears and gut, and we lay the foundations for this ecosystem at birth. According to a new study in the Proceedings of the National Accademy of Sciences (PNAS), different methods of birth (traditional vs cesarean section) have very different outcomes in terms of what bacteria end up colonizing you:

The goal of the present study was to obtain a community-wide perspective on the influence of delivery mode and body habitat on the neonate’s first microbiota[…] We found that in direct contrast to the highly differentiated communities of their mothers, neonates harbored bacterial communities that were undifferentiated across multiple body habitats, regardless of delivery mode. Our results also show that vaginally delivered infants acquired bacterial communities resembling their own mother’s vaginal microbiota, dominated by Lactobacillus, Prevotella,or Sneathia, and C-section infants harbored bacterial communities similar to those found on the skin surface, dominated by Staphylococcus, Corynebacterium, and Propionibacterium.

It’s been known for a long time that c-section babies were more prone to allergies and asthma, and there’s a strong link between commensals and the immune system, but exactly what the difference was remained obscure. Basically, what this paper shows is that the types of bacteria that get us started are established very early.

Babies born through the traditional route are very quickly exposes to the bacterial communities of their mothers – both vaginal and gut bacteria (women often defecate when giving birth). Once these bacteria get established, they fill up all the niches, and prevent other bacteria from getting a foothold. By contrast, c-section babies don’t have this initial exposure – the womb is fairly sterile, and the conditions of this surgery prevent contact with the mother’s other mucosal surfaces. Because of this, the infant is ripe for colonization from the myriad of bacteria found everywhere else, from the nurses and doctors that handle them to the bacteria on the skin on the mother’s breast when feeding.

It’s important to note that we can’t yet draw a distinct causative link between early establishment of bacterial communities and future disease (allergies, asthma etc), right now it’s just correlation. And though infants are colonized by very few types of microbes, as they develop, the microbial ecosystem diversifies into thousands or millions of different species. Researchers are hard at work using new technologies to try to figure out all the different things living in an adult gut (given the spiffy name, “the microbiome”), and we’ve barely scratched the surface.

The one thing that is clear is that the little things living in us and on us can have a profound effect on our health, and with new research, hopefully we can use that knowledge to our advantage.

(Note: This post is not for the squeamish)

All kinds of stuff lives in our guts. It’s been estimated that there are about ten times as many bacteria cells (microflora) in our body as human cells. Most of them are totally harmless, and indeed, they are often beneficial. But as the authors of a paper last week in Science pointed out, bacteria aren’t the only things living down there, and the beasties that live in our gut don’t always play nice, at least, not with us:

The inhabitants of the mammalian gut are not always relatively benign commensal bacteria but may also include larger and more parasitic organisms, such as worms and protozoa. At some level, all these organisms are capable of interacting with each other. We found that successful establishment of the chronically infecting parasitic nematode Trichuris muris in the large intestine of mice is dependent on microflora and coincident with modulation of the host immune response.

Trichuris is a genus of helminth worms that live in the large intestines of mammals. They are wildly successful; over 1 billion (yes, Billion) people are estimated to be infected with T. trichiuria every year. Infection starts with ingesting Trichuris eggs with your food. The eggs are able to survive the harsh environment of your stomach and make their way down to the large intestine, where they hatch and begin feeding, mating, and laying new eggs. When you defecate (we just can’t get away from poo on this blog evidently), the eggs are free to contaminate other food. If you read between the lines correctly, this means that at the beginning of the life-cycle, you must have eaten food contaminated with fecal matter (there’s a reason that this parasite doesn’t do well in regions of the world with good sanitation). This is not nearly as gross as the life-cycle of hook-worms, which can burrow into your foot, swim through your blood-stream to your lungs, then wriggle their way into your mouth through your trachea to be swallowed while you sleep – but I digress.

These researchers wondered what would trigger these ingested Trichuris eggs to hatch. If the worms hatch before they get ingested, they’ll die before they get there, and if they hatch too late, they’ll be expelled before they can establish themselves in the gut. So what is there a lot of in the location they want to hatch, that could provide a signal? Bacteria! When the researchers dumped all kinds of different bacteria on the worm eggs, they hatched. In addition, if they treated mice with high-doses of antibiotics to clear out their guts, and then fed them worm eggs, the worms didn’t hatch. Crucially, dumping bacteria on the eggs only worked if they were at body temperature (37 degrees C); at room temperature, it didn’t work. This makes sense from the worm’s perspective too – there are bacteria everywhere (especially in the poo they’re originally expelled in), but the only place there is likely to be lots of bacteria at 37 degrees is in a mammalian gut.

This doesn’t mean that we should go treating everyone in the 3rd world with antibiotics to prevent worm infections – the normal bacterial flora are too important. But it does raise some potential new lines of preventative therapy. While the exact nature of the interactions between worm egg and bacteria were not complete worked out, they did find that interactions with some types of bacteria were dependent upon a certain class of adhesion molecules, and that these interactions could be blocked by mannose. More understanding of how these different inhabitants of our intestines communicate at the molecular level will doubtless lead to great therapies, but as most of these infections happen in the third world, those therapies will have to be cheap if they’re to do any good.