Gut Microbiota: Our Native Flora
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Since the emergence of sponges some 500 million years ago, animals have coexisted with microorganisms. In humans, they colonize from head to toe, forming complex ecological communities, interacting with one another and with human cells. They are extremely varied, with scientists identifying more than 1,000 species belonging to more than 50 different phyla, or “tribes.” Although most are bacteria, a few are fungi, viruses and other organisms called protists, which resist easy classification. So far, we know that these organisms synthesize vitamins; stimulate development of tissues, including parts of the gastrointestinal tract, the cecum and some lymphatic tissues; and protect us from pathogenic bacteria by competing with them for nutrients and attachment sites, by stimulating production of antibodies and, possibly, by secreting substances that destroy or inhibit certain pathogens.
Micah Lidberg
With growing knowledge about the microbes in and on people have come key tenets defining the microbes’ relationship with human hosts. They have evolved alongside us, with ongoing natural selection for bacteria that benefit both humans and their own species. And some microbes colonize specific parts of the body. E. coli inhabit the colon, lactobacilli colonize the vagina, and staphylococci live on the skin. Researchers often refer to resident microbiota as commensals, meaning that their presence doesn’t harm us—the word, from Latin, means “eating at the same table.” But research has revealed that a single bacterium can have both beneficial and harmful effects. For example, although in most people H. pylori has lived as a commensal, in some it creates a painful, damaging stomach ulcer.
Yet just as scientists begin to skim the surface of what humans’ resident bacteria are and what they might be doing, they’re also finding that the bugs are changing—sometimes dramatically, as in the case of H. pylori. To Blaser and others, its rapid disappearance seems to be linked to major changes in human ecology. As Blaser and his colleague Stanley Falkow, a professor of microbiology and immunology at Stanford University School of Medicine, laid out in an essay in Nature Reviews Microbiology, during the past few generations we’ve limited our bacterial exposure by living in smaller families, having less contact with other people (contact that used to come via shared beds, closer living quarters and communal food) and consuming cleaner water and food. Increasingly common cesarean section births deprive babies of the chance to be colonized with their mothers’ bacteria as they pass through the birth canal; meanwhile, breast-feeding—another rich source of microbes—significantly declined during the first half of the 20th century, though it has rebounded somewhat since the 1970s. And antibiotics, particularly in children, can wipe out swaths of microbial residents with one course of treatment.
These changes amount to a threat to our microbes’ existence and a reason to evolve new defenses that may have unhappy consequences for their human hosts. “They’ve adapted,” presumably by changing their genes, says Foxman, “because they live and evolve on such a short life span—producing new generations in minutes or days—while our genes have not.”
