Scientists have long studied the link between our genes and our health. Now, in a growing area of scientific research, they’re studying the link between the bacteria in our intestines and virtually every disease that ails us.
Helicobacter pylori may be the most successful pathogen in human history. While not as deadly as the bacteria that cause tuberculosis, cholera, and the plague, it infects more people than all the others combined. H. pylori, which migrated out of Africa along with our ancestors, has been intertwined with our species for at least two hundred thousand years. Although the bacterium occupies half the stomachs on earth, its role in our lives was never clear. Then, in 1982, to the astonishment of the medical world, two scientists, Barry Marshall and J. Robin Warren, discovered that H. pylori is the principal cause of gastritis and peptic ulcers; it has since been associated with an increased risk of stomach cancer as well. Until that discovery, for which the men shared a Nobel Prize, in 2005, stress, not an infection, was assumed to be the major cause of peptic ulcers.
Dysbiosis of the intestinal microbiota affecting the gut barrier could be triggering Type 1 Diabetes (T1D), the second most frequent autoimmune disease in childhood. This study compared the structure of the fecal microbiota in 29 mestizo children aged 7–18 years, including 8 T1D at onset, 13 T1D after 2 years treatment, and 8 healthy controls. Clinical information was collected, predisposing haplotypes were determined; the fecal DNA was extracted, the V4 region of the 16S rRNA gene amplified and 454-pyrosequenced. The newly diagnosed T1D cases had high levels of the genus Bacteroides (p , 0.004), whereas the control group had a gut microbiota dominated by Prevotella. Children with T1D treated for $2 years had levels of Bacteroides and Prevotella compared to those of the control group. The gut microbiota of newly diagnosed T1D cases is altered, but whether it is involved in disease causation or is a consequence of host selection remains unclear.