This study was carried out in genetically modified mice prone to getting type 1 diabetes and which also lacked a part of the immune system involved in bacterial response. It found that 80% of mice given antibiotics to be kept germ-free, developed diabetes, and mice exposed to a mixture of normal gut bacteria developed substantially less diabetes. These results have been over-interpreted by the newspapers and it is not clear whether these results are truly representative of the development of diabetes in humans. Resident bacteria are a normal part of the human body and would not be expected to be destroyed by maintaining a clean house.

Where did the story come from? Dr Li Wen from the Yale University School of Medicine and colleagues from the Washington University School of Medicine, University of Chicago, University of California San Francisco in the US, and the UK’s Bristol University carried out the research. The study was supported by numerous institutional grants to individual researchers. The study was published in the peer-reviewed scientific journal: Nature.

What kind of scientific study was this? The researchers say that there has been a rise in the incidence of type 1 diabetes in developed countries over the past few decades and that this increase may be a result of changes in the human environment, including human exposure to microbes.

To investigate this, they carried out a number of experiments on a certain strain of mice called non-obese diabetic (NOD) mice. This strain of mice have been developed to be susceptible to developing type 1 diabetes and this predisposition is influenced by the animals’ living environment and also through being directly exposed to microbes by being injected with pathogens.

This was a laboratory study in which the researchers carried out a large number of experiments to look at the relationship between microbes, certain proteins involved in the immune response, and the development of type 1 diabetes in these NOD mice.

In their first experiment, the researchers used a group of NOD mice that were genetically modified to lack the MyD88 protein, which plays a role in the functioning of several microbe receptors in the immune system. The mice were kept under normal conditions, free of any mouse pathogens (disease-causing microbes), and monitored to see if they developed type 1 diabetes (which they would normally). Similar experiments were also carried out in other genetically modified mice to investigate whether removing individual microbe receptors in the immune system had an effect on the development of diabetes in the NOD mice, and what type of immune cells might be involved.

The results of these initial experiments led the researchers to suspect that intestinal bacteria could affect the diabetic resistance of NOD mice without the MyD88 protein. To investigate this possibility, they treated another group of NOD mice without MyD88 with an antibiotic throughout their lifetime to make them bacteria-free. They then compared the number that developed diabetes between this group, a group without MyD88 that had not been treated with antibiotics and a group that had MyD88 and were treated with antibiotics.

To demonstrate that the development of type 1 diabetes was affected by a lack of microbials, the researchers treated MyD88-lacking NOD mice with antibiotics to remove bacteria, then colonised them with a cocktail of typical gut bacteria (based on a sample analysed in a gut specimen). They also exposed the offspring of germ-free NOD mice to MyD88-lacking mice, so that they would be exposed to bacteria, and looked at whether they developed diabetes at up to eight weeks of age.

What were the results of the study?]]>The researchers found that NOD mice lacking the MyD88 protein did not spontaneously develop type 1 diabetes under normal conditions. They also found that MyD88-lacking NOD mice that were given antibiotics so that they were germ-free developed diabetes more frequently than the MyD88-lacking NOD mice who were not treated with antibiotics. Treatment with antibiotics did not affect diabetes development in NOD mice that had MyD88.

However, when the germ-free MyD88-lacking mice were exposed to bacteria normally present in the human gut, the development of type 1 diabetes reduced, with only 34% of male mice becoming diabetic compared to over 80% of the still germ-free MyD88-lacking NOD mice. Antibiotic treatment was found to alter ratios of different types of bacteria in the mouse gut, and a lack of MyD88 protein in itself was found to affect the composition of normal bacteria in the gut. Exposure to bacteria from MyD88-lacking NOD mice also reduced the development of diabetes in young NOD mice with the MyD88 protein that would normally develop diabetes.

What interpretations did the researchers draw from these results? The researchers conclude that the interaction of intestinal microbes with receptors in the immune system is a critical factor affecting the development of type 1 diabetes.

What does the NHS Knowledge Service make of this study? This was a study in genetically modified mice that were predisposed to getting diabetes and also lacked a part of the immune system that is involved in bacterial response. It found that 80% of mice treated with antibiotics in order to be kept germ-free, developed diabetes, and that exposure to a mixture of normal gut bacteria resulted in substantially less developing diabetes. These results have been over-interpreted by the newspapers. It is not yet clear to what extent these genetically modified mice are representative of the development of an autoimmune condition such as diabetes in humans.

Normal bacteria that live in the human gut are likely to be very different from those that live in the mouse gut. Even if, as researchers now aim to investigate, certain gut bacteria have a protective effect against diabetes, resident bacteria are a normal part of the human body and would not be expected to be destroyed by maintaining a clean house.

In type 1 diabetes the body’s immune system destroys its own insulin-producing cells. The exact causes are not known but may include genetic factors, other autoimmune conditions and environmental exposures such as viruses or other toxins. Further research into the effects of normal gut bacteria on the development of type 1 diabetes is expected.

]]>The researchers found that NOD mice lacking the MyD88 protein did not spontaneously develop type 1 diabetes under normal conditions. They also found that MyD88-lacking NOD mice that were given antibiotics so that they were germ-free developed diabetes more frequently than the MyD88-lacking NOD mice who were not treated with antibiotics. Treatment with antibiotics did not affect diabetes development in NOD mice that had MyD88.

However, when the germ-free MyD88-lacking mice were exposed to bacteria normally present in the human gut, the development of type 1 diabetes reduced, with only 34% of male mice becoming diabetic compared to over 80% of the still germ-free MyD88-lacking NOD mice. Antibiotic treatment was found to alter ratios of different types of bacteria in the mouse gut, and a lack of MyD88 protein in itself was found to affect the composition of normal bacteria in the gut. Exposure to bacteria from MyD88-lacking NOD mice also reduced the development of diabetes in young NOD mice with the MyD88 protein that would normally develop diabetes.

What interpretations did the researchers draw from these results? The researchers conclude that the interaction of intestinal microbes with receptors in the immune system is a critical factor affecting the development of type 1 diabetes.

What does the NHS Knowledge Service make of this study? This was a study in genetically modified mice that were predisposed to getting diabetes and also lacked a part of the immune system that is involved in bacterial response. It found that 80% of mice treated with antibiotics in order to be kept germ-free, developed diabetes, and that exposure to a mixture of normal gut bacteria resulted in substantially less developing diabetes. These results have been over-interpreted by the newspapers. It is not yet clear to what extent these genetically modified mice are representative of the development of an autoimmune condition such as diabetes in humans.

Normal bacteria that live in the human gut are likely to be very different from those that live in the mouse gut. Even if, as researchers now aim to investigate, certain gut bacteria have a protective effect against diabetes, resident bacteria are a normal part of the human body and would not be expected to be destroyed by maintaining a clean house.

In type 1 diabetes the body’s immune system destroys its own insulin-producing cells. The exact causes are not known but may include genetic factors, other autoimmune conditions and environmental exposures such as viruses or other toxins. Further research into the effects of normal gut bacteria on the development of type 1 diabetes is expected.

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