Antibiotics ‘put people at risk of flu’

Antibiotics ‘put people at risk of flu’ because they ‘turn off’ immune signals that help the body fight off the virus in the lungs

  • Mice that ‘overproduce’ these signals are less likely to catch flu
  • And those that do become infected, fight the virus off quicker 
  • Two weeks of antibiotics reduced these signals, leaving the rodents at risk 

Antibiotics could be putting people at risk of flu, research suggests.

A study found the life-saving drugs ‘turn off’ signals in the lung cells of mice that prevent the virus replicating.

Rodents that ‘over produced’ these signals, called baseline type I interferon (IFNα/β), were less likely to catch flu. And those that did become infected fought the virus off quicker.

But just two weeks of antibiotics reduced these interferon signals, leaving the animals at a higher risk of infection. 

This was reversed again by a faecal transplant from healthy mice, which suggests IFNα/β is driven by the microbiome. 

Researchers warn taking antibiotics ‘inappropriately’ could wipe out the good bacteria in our gut that keep us healthy and virus-free.

Antibiotics could be putting people at risk of flu, research suggests (stock)

The research was carried out by the Francis Crick Institute, a biomedical research centre in London. It was led by Andreas Wack, group leader of the immunoregulation laboratory.

‘This study supports that taking antibiotics inappropriately not only promotes antibiotic resistance and wipes out the commensals in your gut that are useful and protective,’ Dr Wack said.

‘But it may also render you more susceptible to viral infections.

‘In some countries, the livestock industry uses antibiotics a lot, prophylactically, so treated animals may become more susceptible to virus infections.’

Inappropriate antibiotic use may include taking the drugs for viruses, for which they are ineffective, or not completing the full course of treatment as prescribed.

This enables bacteria to evolve resistance to antibiotics, rendering them useless.

While the EU restricts antibiotics in agriculture, countries like the US allow farmers to give livestock a low dose of the drugs to prevent illness and even promote growth. 

This increases the risk of antibiotic-resistant strains of bacteria infecting consumers and animals. The ‘superbugs’ could also contaminate soil and waterways. 

When fighting a virus, our bodies fire up IFNα/β signals, which trigger inflammation.

These signals are fine-tuned to kill the virus without harming healthy tissue.

This trade-off is seen in people with genetic mutations that increase their number of IFNα/β receptors, leading to widespread inflammation.

WHAT IS ANTIBIOTIC RESISTANCE?

Antibiotics have been doled out unnecessarily by GPs and hospital staff for decades, fueling once harmless bacteria to become superbugs. 

The World Health Organization (WHO) has previously warned if nothing is done the world is heading for a ‘post-antibiotic’ era.

It claimed common infections, such as chlamydia, will become killers without immediate solutions to the growing crisis.

Bacteria can become drug resistant when people take incorrect doses of antibiotics or if they are given out unnecessarily. 

Chief medical officer Dame Sally Davies claimed in 2016 that the threat of antibiotic resistance is as severe as terrorism.

Figures estimate that superbugs will kill 10 million people each year by 2050, with patients succumbing to once harmless bugs.

Around 700,000 people already die yearly due to drug-resistant infections including tuberculosis (TB), HIV and malaria across the world. 

Concerns have repeatedly been raised that medicine will be taken back to the ‘dark ages’ if antibiotics are rendered ineffective in the coming years.

In addition to existing drugs becoming less effective, there have only been one or two new antibiotics developed in the last 30 years.

In September, the WHO warned antibiotics are ‘running out’ as a report found a ‘serious lack’ of new drugs in the development pipeline.

Without antibiotics, C-sections, cancer treatments and hip replacements will become incredibly ‘risky’, it was said at the time.

To investigate how this delicate balance is maintained, the researchers analysed mice with a mutation that caused them to ‘overproduce’ IFNα/β. 

The rodents were then exposed to the flu virus.

Results – published in the journal Cell Reports – revealed these animals were more resistant to the pathogen.

Of those that did get infected, they showed a reduced ‘viral load’ eight hours after being exposed.  

And after two days, the virus had not ‘taken hold’ to the same extent as it does in other mice.  

The rodents also experienced less weight loss, which can be a symptom of flu.

Due to the ‘viral load’ being controlled early on, a subsequent immune response never fully kicked in.

This initially suggested that regulating IFNα/β receptors could help fine-tune anti-viral signals in the fight against flu.

However, this protective effect started to diminish after the mice were on antibiotics for two to four weeks. 

The treatment reduced IFNα/β signalling, particularly in lung stromal cells, which make up the connective tissue that surrounds the organ.

But giving the mice a faecal transplant reversed this back again, with IFNα/β signalling becoming strong. 

Faecal transplants aim to boost a recipient’s gut bacteria levels and diversity by taking purified stool samples from a healthy donor. 

The overall results suggest the microbiome plays a role in IFNα/β signalling, which then helps to protect against flu.

This is consistent with past findings that show treating mice with oral antibiotics makes them more susceptible to viruses. 

‘This and previous studies demonstrate that microbiota-driven signals can act at multiple levels,’ Dr Wack said.

‘[The signals] induce an antiviral state to control infection early on, enhancing the functionality of immune cells later in infection.’

The researchers hope to uncover the exact mechanisms that cause gut bacteria to drive resistance to viral infections.

‘Previous research has suggested the microbiota-driven signal in lung stromal cells could originate either from the gut or the lung,’ Dr Wack said. 

‘However, in the work presented here, the results of the fecal transplant experiments strongly suggest a gut involvement in this effect. 

‘We would love to understand the exact nature of the signal from the gut to the lung, and we are working on several hypotheses.’

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