The research focused on the microbiome, the bacterial species in our guts that co-evolved with humans to play roles in digestion, metabolism and immunity, researchers from New York University (NYU) in the US said.
As children's exposure to microbe-killing antibiotics has increased in recent decades, the incidence of autoimmune diseases like Type 1 diabetes has more than doubled.
The study found that short pulses of antibiotics cause mice that are susceptible to Type 1 diabetes to develop the disease more quickly and more often.
"This work uses non-obese diabetic (NOD) mice, the best model of type 1 diabetes to date, and doses of antibiotics like those received by most children to treat common infections," said Blaser.
This is the first study of its kind suggesting that antibiotic use can alter the microbiota and have lasting effects on immunological and metabolic development, resulting in autoimmunity, said Jessica Dunne from NYU.
Researchers assessed the effects of antibiotic treatment on the development of microbiomes in NOD mice, which are known to be more susceptible to Type 1 diabetes.
Specifically, male NOD mice exposed to PAT were found to have twice (53 per cent) the incidence of Type 1 diabetes as control NOD mice (26 per cent incidence) that received no antibiotics, researchers said.
To determine the effects of antibiotics, researchers collected samples of gut bacteria from all study mice.
They used genomic and statistical techniques to analyse the millions of pieces of bacterial DNA in the samples.
Three-week-old PAT males, for instance, had a nearly complete loss in their intestines of certain bacteria shown in past studies to normally train the immune system.
The results, which produced immunological changes resembling those seen in the microbe donors, showed that a perturbed microbial population by itself was sufficient to alter the recipient's immune system.
The findings were published in the journal Nature Microbiology.
Disclaimer: No Business Standard Journalist was involved in creation of this content
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