Autoimmune disorder lupus may be triggered by body’s bacteria

Disturbances in the body’s microbiome have already been linked to plenty of disorders, including autoimmune diseases * (down details), which occur when a person’s immune system starts to attack their own body. In people with lupus, this kind of attack often causes skin rashes, but can also damage other organs, such as …

Our Own Microbiome Might Be Triggering The Autoimmune Disease Lupus

We already know that the bacteria that live on and within us are far more than just inert passengers. They interact with our cells and are associated with a whole host of conditions and diseases. Now, researchers think that our microbiome might also play a role in the autoimmune disease lupus.

Currently, there is no cure for systemic lupus erythematosus, or lupus for short. It occurs when the body’s immune system goes out of whack and starts attacking healthy tissue, causing joint problems, tiredness, skin rashes, and in severe cases inflamed kidneys, lungs, and even the brain. It is still not fully understood what causes it, but a new study published in Science Translational Medicine finds that the bacteria inside us might at least contribute to it.

We already know that when lupus flares up, the immune system turns on the body and starts attacking Ro60, a protein that is also known to be produced by some bacteria living in soil. The researchers therefore decided to look to see if the bacteria in people also produced this protein, and it turns out they do. What is more, for those with lupus, Ro60 seemingly triggered an immune response.

They then took bacteria that produce a similar protein to Ro60 and put it in mice bred without a microbiome. The result was that the mice developed signs of kidney failure, a similar response to what happens to people with lupus.

“We don’t really know what causes lupus, but it is thought to be a combination of genetics, environment and hormones,” Martin Kriegel, from Yale School of Medicine, told New Scientist.

From these experiments, they suspect that those who have lupus have an underlying genetic susceptibility to Ro60, and so when the bacteria produces it, their immune system goes into overdrive.

While we can’t – for the time being at least – change the genetics, we can alter the community of bacteria living within someone. This is looking like it could become the best way to treat patients with lupus, although as Kriegel points out, we’re still not there yet.

Current antibiotics to treat the gut microbiome are simply too general to be of much use here. What the researchers are now hoping to explore is a far more targeted drug that precisely hits only the bacteria making the protein and nothing else.

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autoimmune diseases

People who have autoimmune disorders may be 20 per cent more likely to develop dementia. That’s according to an analysis of 1.8 million hospital cases in England.

Based on data collected between 1999 and 2012, the study’s findings add to mounting evidence that chronic inflammation – a common feature of many autoimmune disorders – may be a trigger of dementia and Alzheimer’s disease.

Previous studies have found that if infections or chronic inflammatory diseases – including diabetes – have pushed a person’s immune system into overdrive, this can lead to immune cells attacking healthy brain tissue.

Varying effect

According to the analysis, people with multiple sclerosis are among those with autoimmune disorders who are most likely to develop dementia. This finding isn’t very surprising, as the disorder is caused by the immune system attacking the central nervous system. The study, led by Michael Goldacre at the University of Oxford, found that people with the condition have double the risk of developing dementia.

But other autoimmune disorders were also associated with rises in dementia risk. The skin condition psoriasis was linked to a 29 per cent increase, while the risk of developing dementia was 46 per cent higher in people who have lupus erythematosus, a disorder that involves rashes and fatigue.

However, people with rheumatoid arthritis turned out to have around a 10 per cent lower risk of dementia. This could be because many people with arthritis take non-steroidal anti-inflammatory drugs, such as aspirin and ibuprofen, which may tame inflammation that could otherwise contribute to causing dementia.

“They reduce inflammation and that could explain why there’s less spillover, at least in principle,” says Goldacre.

Heart and head

His team also found a strong link between autoimmune disease and heart and circulatory problems. Overall, people with autoimmune disease were 53 per cent more likely to be admitted to hospital due to cardiovascular disease, and 46 per cent more likely to be admitted for a stroke.

This may explain a large part of the increased dementia risk in people with autoimmune disorders. Vascular dementia is a kind of dementia that involves poor blood flow in the brain. When Goldacre and his team looked specifically at different kinds of dementias, they found that people with autoimmune diseases are 29 per cent more likely to develop vascular dementia, but only 6 per cent more likely to get Alzheimer’s disease.

“It’s striking that increased risk for vascular dementia exceeds that for Alzheimer’s,” says Colm Cunningham at Trinity College Dublin, Ireland. “The impact of autoimmune diseases on cardiovascular disease may be the key common link.”

Nevertheless, the relatively smaller increase in Alzheimer’s risk associated with autoimmune conditions may help researchers understand this disease better. “The results are very compelling and support the notion that neurovascular damage and inflammation are key drivers of risk for Alzheimer’s disease,” says leading Alzheimer’s researcher Rudolph Tanzi, at Massachusetts General Hospital in Charlestown.

For those looking to reduce dementia risk by controlling their inflammation levels, Goldacre says exercise and a healthy diet may help. “These are good for avoiding Alzheimer’s, but for all sorts of other benefits too,” he says.

Journal reference: Journal of Epidemiology & Community Health, DOI: 10.1136/jech-2016-207809

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