Max Planck Institute for Infection Biology, Berlin, Germany.

A microbiologist wonders how antimicrobial peptides beat infection.

My group is interested in why, although people often pick up infections and sometimes become ill, they almost always recover. Recovery is the result of a fantastically efficient immune system that relies in part on proteins and peptides that kill microbes.

Antimicrobial peptides were discovered in systematic searches for potential drugs, and there are several types. Most are cationic and bind to the anionic surface of microbes. Recently, Roberto Lande at the University of Texas in Houston and his colleagues convincingly showed that one antimicrobial peptide, LL-37, can also bind DNA and serve as an activator for other immune cells (R. Lande et al. Nature 449, 564–569; 2007).

LL-37 is one of several antimicrobial peptides that do more than kill microbes and activate immune cells. Its other functions include chemoattraction and wound repair. But, as its name indicates, LL-37 has only 37 amino acids. It is plausible that its multiple effects on the host are due to its interaction with specific receptors that, in combination with other signals, result in diverse biological functions. More intriguing, however, is the fact that LL-37 kills microbes in the first place.

The question is whether LL-37 and other antimicrobial peptides truly function as bacterial killing agents in the host. Their antimicrobial activity has so far been demonstrated only in vitro, where it might be a reflection of their cationic character. Another more attractive possibility is that infections are such an important threat to the host that, during evolution, many cationic proteins with diverse function were co-opted to serve as antimicrobial agents. If we do have many ways to kill microbes, maybe it is not so surprising that we often recover from infections.

Posted by Brendan Maher at 06:44 PM | Permalink | Comments (0) | TrackBacks (0)

University of British Columbia, Vancouver, Canada

A microbiologist wonders where diversity comes from.

Recent estimates indicate that the total number of bacteria in the biosphere approaches or exceeds 10 to the power 31. A major goal of microbiology is to understand what creates their diversity and how it is maintained.

Having trained as an organic chemist, I came to appreciate microbial diversity through the extravagance of small molecules that microbes produce. This reflects a diversity in microbial metabolism, which one might expect to have evolved as a result of the (organic) richness of the organisms' environments. But a couple of recent publications present findings that do not sit easily with this view.

Our first inkling of the huge diversity of the microbial world came from the use of ribosomal-RNA typing in the late 1980s. In the 1990s, this morphed into the expanding field of metagenomics, which is now providing catalogues of microbial communities from diverse terrestrial and marine environments.

One comparison of such catalogues showed that the seemingly bare and boring Arctic tundra exceeds fertile forest soils in phylogenetic content (J. D. Neufeld and W. W. Mohn Appl. Environ. Microbiol. 71, 5710–5718; 2005). A more recent study compared information from more than 100 different environments, finding that the microbial content of soils is generally less diverse than that of sediments and hypersaline environments (C. A. Lozupone and R. Knight Proc. Natl Acad. Sci. USA 104, 11436–11440; 2007).

I am looking forward to seeing what happens when the Human Microbiome Project gets under way. What variety of microbes is there to find living within us? What are they all doing? In what way will the population depend on diet? Given that we don't yet seem to understand the relationship between diversity and ecology, I am making no predictions.

Posted by Jenny Hogan at 06:00 PM | Permalink | Comments (3) | TrackBacks (0)

Liverpool John Moores University, UK

An ecologist enjoys a smelly experiment on a neglected link in the food web.

I have long been fascinated by an idea from the 1970s about rotting food. Daniel Janzen, now at the University of Pennsylvania in Philadelphia, suggested then that many of the noxious chemicals secreted by microbes in decaying food are produced to fend off large animals, allowing the microbes to keep the resource for themselves.

It's an intuitively appealing hypothesis. Our own experience is to be repulsed by putrid food, and several studies have shown that birds prefer fresh over rotted fruit. Most recently, a careful study in the seas off the southeasten United States provided further support for Janzen's idea (D. E. Burkepile et al. Ecology 87, 2821–2831; 2006).

In what must have been a gloriously smelly experiment, the researchers baited crab traps with dead fish, either rotten or fresh. The microbe-laden carrion was four times less likely to be consumed by scavengers than the fresh fish.

This provides clear evidence that microbes compete for food with larger animals, something that has been largely overlooked in the huge ecological literature on food webs and feeding relationships. But it doesn't tell us how the chemicals evolved.

Last year, I published with colleagues a theoretical analysis of the evolutionary implications of Janzen's idea (T. N. Sherratt et al. Ecol. Modell. 192, 618–626; 2006). Our model suggested that the chemicals cannot have evolved solely to protect against large animals, because the temptation for microbes to 'cheat' by free-riding on toxin production by others undermines the system.

The experiments done by Burkepile et al. show that the effect is real, but perhaps these chemicals first evolved for other reasons, such as inter-microbe competition?

Posted by Jenny Hogan at 06:00 PM | Permalink | Comments (2) | TrackBacks (0)