The Next Big Antibiotic Could Come from the Gut of an Insect
No one can dispute the evolutionary success of bugs. The oldest insect fossils were found encased in crystallized mineral silica in Scotland in 1926, and they're between 396 and 407 million years old.
Insects have seen dinosaurs come and go. They have survived disruptions to the Earth's weather, atmosphere, and land formations that caused extinction of other species. They have survived human's best efforts to eradicate them.
Yet almost a half billion years later, they are still with us.
Scientists have attributed part of insects' survival to a combination of several characteristics. An exoskeleton, small size, ability to fly, tremendous reproduction potential (female insects lay and average of 100-500 eggs in a lifetime), metamorphic development stages, and genetic adaptability all contribute to keeping the million species of insects alive and well and inhabiting the earth.
Research published in the January 19 issue of Cell Chemical Biology reported on a novel way insects can create their own survival advantage—by making and secreting their own antibiotic to combat pathogenic bacteria they ingest.
Even though about half of the insect species are herbivores, they eat their share of the bacteria which freeload on plants.
To investigate how insects face these pathogens unscathed, lead author, Wilhelm Boland, from the Max Planck Institute for Chemical Ecology in Jena, Germany, and his colleagues, turned to the cotton leafworm, aka Spodoptera littoralis, a common inhabitant of temperate regions with a voracious appetite for causing crop destruction.
Since the cotton leafworm consumes so much plant material, the researchers knew they must ingest infectious bacteria, as well.
Their study examined the gut bacteria in the cotton leafworm as it developed. They found that the gut of young worm larvae were colonized with a potentially pathogenic Enterococcus, but older larvae guts were colonized primarily by Enterococcus mundtii—a bacteria not known to be dangerous to the insects.
Studies into the cause of the shift from one Enterococcus type to another led the researchers to discover that E. mundtii produces a peptide—a piece of a protein—and this one had antimicrobial properties. This peptide, mundticin KS, strongly inhibited some potentially pathogenic organisms.
The real survival benefit finding was that mundticin KS was active against invading bacteria, but not against gut bacteria the insects needed for digestion and other metabolic functions.
Besides a distinct survival mechanism for insects, the study authors made several suggestions about ways this mechanism could be used by humans.
Understanding the role of indigenous gut residents will contribute to the development of novel biocontrol strategies against herbivorous insect pests. Our observation that insects successfully rely on peptide antibiotic against enterococcal infections also has implications for the struggle against rapidly emerging multi-drug-resistant enterococcal pathogens in humans.
To hedge our long-term survival, humans might take a lesson from our insect friends and create our own strategies to adapt—exploiting the techniques insects have already developed.