The (soil) cycle of life

Decomposition is a great housekeeper: it takes care of dead plants and animals by breaking them down into simple molecules.  A variety of fungi, insects, worms, and bacteria are involved in decomposition.  The end result is that nutrients are returned to the soil for use by the next generation of plants.

Decomposition is important for maintaining the ecosystem, because there is a finite amount of matter in the world.  Think of it like a bunch of Legos: you can build a whole town, but then all your bricks are used up.  To build something new, you have to take apart the cars and buildings that you’re done playing with.  Then you can build something else with the freed-up pieces.

If you live in a town or city, you might not think about decomposition very often.  But out in the woods, you can’t miss it.  You’re often tromping on a thin layer of dead leaves that are square in the middle of being decomposed.  It’s long been thought that the main factor affecting the return of nutrients to the soil was simply how many plants were around to be decomposed.

Turns out it might be more complex than we thought.  In a study published in Science on June 15th 2012, Dror Hawlena, a post-doc in the Schmitz lab at the Yale School of Forestry, and his colleagues show that the rate of plant decomposition is affected by the predators in an ecosystem.

And it’s not because predators are eating the plants.

Hawlena and his colleagues stressed grasshoppers by raising them with a natural predator: a spider, but one whose mouth was glued shut.  The grasshoppers were under the impression that they could be dead at any minute.  Grasshoppers lived their lives, with or without the spiders present, died, and decomposed by the hand of microbes in the soil.

When prey animals, like grasshoppers, feel their lives are in danger, they want a constant supply of ready energy in case they have to make a break for it.  So, they eat more carbohydrates and break proteins in their bodies down into sugar.  While these behavioral and metabolic changes give the grasshoppers energy, they also alter the chemical composition of their bodies.  Carbohydrates have lots of carbon and not a lot of nitrogen, and the proteins that they dismantled were loaded with nitrogen. The combined effect of these changes is that stressed grasshoppers have a higher carbon-to-nitrogen ratio than unstressed grasshoppers.  Dead grasshoppers become part of the microbial diet.  True to the old adage, “you are what you eat,” that carbon/nitrogen imbalance is passed on to the microbes.

When the researchers piled dead grass on top of the soil where the grasshoppers had been, they found a surprise: microbes that broke down stressed grasshoppers were 200% less efficient at breaking down the grass.  The reason this is so surprising is that there was only a 4% difference in the carbon-to-nitrogen ratio between stressed and unstressed grasshoppers.  That small difference in body chemistry exploded into a huge effect on the rate of plant decomposition.

So, microbes eating stressed grasshoppers get less nitrogen.  Nitrogen is what microbes use to grow and to make the enzymes that break down dead plants.  Less nitrogen in the microbial diet probably means fewer microbes and fewer digestive enzymes in the soil, hence slower decomposition.

This doesn’t mean that we should mount a campaign against grasshopper stress.  Nature has a way of finding the right balance when left to its own devices.  But humans have a way of mucking with nature, so we need to keep in mind that the endangerment or extinction of high-level predators could have a ripple effect on the entire ecosystem; one that reaches deeper than we originally thought.


More reading:

Fear of predation slows plant-litter decomposition. Science. 2012 Jun 15;336(6087):1434-8.


Stay, bacteria…stay

We are teeming with bacteria, fungi, and viruses.  This is a deliberate arrangement that every one of us unwittingly enters into.  From the moment we are born, we begin to accumulate and cultivate certain desired microbes.  They live without and within, on our skin and in our guts.  We co-evolved with the microbes and it’s a mutually beneficial relationship.

In our intestines, microbes help us with digestion and nutrition.  They give us access to the energy stored in some complex carbohydrates that would otherwise just pass through.  They make the vitamin K that we need. For that, we give them room and board.  It’s a happy relationship.

But these are bacteria, viruses, and fungi.  Those are the same words ascribed to infections and disease.  How do we make this work?

In order to safely contain these microbes, we have constructed barriers and safeguards that separate what’s going on in the gut from the rest of the body.  The gut is lined by epithelial tissue with tight junctions between cells to prevent microbes from slipping through.  The thick layers of mucous secreted into the intestines are hard for microbes to cross.  In that mucous are gut-specific immune cells.  They deal with surveying the massive numbers of bacteria within the gut, and reporting back to gut’s immune tissue.  Any hardy invaders that bypass these defenses should be picked up by the gut’s lymphatic tissue. Ideally, problems are dealt with before the body’s general immune system has to get involved, which would lead to system-wide infection and inflammation.

The tissue and mucous barriers that restrict microbes to the guts are physical barriers, like walls. In a paper published by David Artis’s group at the University of Pennsylvania in Science on June 8th, 2012, scientists describe the first non-physical barrier known to keep microbes in their place.  They found that cells of the immune system secrete a signal that prevents a bacteria called Alcaligenes from being spread throughout the body.

Alcaligenes are relegated to the gut’s immune tissues: Peyer’s Patches and mesenteric lymph nodes, which sit on the other side of that epithelial wall.  They sample what sneaks through, keeping a watchful eye out for foreign invaders.  So, the same tissues that constantly patrol for invading bacteria have selected one to let in, and they work to keep it there.

In the lab, Alcaligenes are known to secrete antimicrobials that can kill some E. coli, Strep, and Staph.  Maybe that’s why the gut has invited these bacteria to call our bodies home.  It may be of extra benefit to have them in the Peyer’s Patches, where immune cells sit in wait for foreign invaders.  Like a team, the immune cells can detect an invasion, and the Alcaligenes might help eliminate it.

These lymph nodes sit next to the intestines, straddling that physical barrier that our body erected to keep the microbes that help us with digestion from crossing into the rest of the body.  So how do we confine the Alcaligenes to those places, if they’re on the other side of the wall?

Innate lymphoid cells, that’s how.  Researchers found that innate lymphoid cells secrete a signal, the cytokine IL22, which keeps Alcaligenes in the lymphatic tissue of the gut.  When innate lymphoid cells are taken out of the picture, the Alcaligenes disperse throughout the body.  Treating mice that are missing innate lymphoid cells with IL22 keeps the Alcaligenes in their place, so it appears to be the secretion of IL22 that contains the Alcaligenes.

If the Alcaligenes escape the gut, the adaptive immune system mounts a response to eliminate them.  In the lab, two weeks after Alcaligenes escaped their gut confinement, the only thing remaining were antibodies specific to the bacteria, patrolling for more. But the mice weren’t necessarily good as new.  The mice had residual systemic inflammation following the infection.

This research could have bearing on people with chronic or inflammatory diseases.  Patients with Crohn’s disease, cancer, HIV, and Hepatitis C infection are more likely to have experienced a system-wide Alcaligenes infection.  If we can prevent Alcaligenes from leaving the gut, we may be able to limit inflammation in chronic human diseases, which would improve patient outcome.  It’s also another surprising role for innate lymphoid cells, which were only discovered about ten years ago.  Scientists are still teasing apart their varied functions.  It’s a mixed bag so far.  The cells have been implicated as helpful in recovering from the flu and initiating immune responses, to harmful in colitis and asthma.  We can add this discovery to the growing list of potential therapeutic targets to treat inflammatory disease.


More reading:

There’s a collection of articles on the Science website about the microbiome.  And it’s free to anyone in the month of June…a step in the right direction towards open access.

Innate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria, Science, vol. 336, 8 June 2012.

Indigenous opportunistic bacteria inhabit mammalian gut-associated lymphoid tissues and share a mucosal antibody-mediated symbiosis, PNAS, vol. 107:16, April 20, 2010.

Crossover immune cells blur the boundaries, Science 8 June 2012: Vol. 336 no. 6086


Photo credit: Thanks to Euthman for the great histology pic on Flickr, kindly available under the Creative Commons license.