Doctors already know that misusing antibiotics can cause antibiotic resistance, which can make it difficult to fight bacterial infections, such as pneumonia. Now, a study in mice suggests that antibiotic use could also make the lungs more vulnerable to viral infections, such as the flu.
Antibiotic resistance has become a pressing issue for researchers and healthcare professionals. This phenomenon occurs when a bacterial infection no longer responds to the antibiotics that doctors typically use to treat it.
This resistance often develops due to the misuse or overuse of antibiotics, as many individuals across the world mistakenly opt for antibiotics to treat viral infections, such as the influenza virus which causes the flu, against which these drugs are ineffective.
A new study in mice by researchers from the Francis Crick Institute in London, United Kingdom, now suggests that antibiotics could actually also ‘prepare’ the lungs for viral infections. The researchers’ findings also show that gut bacteria drive a type of protein signaling that helps the cells that line the lungs keep the flu virus from spreading.
In the new study, researchers used a group of mice with healthy gut bacteria at baseline. Over 4 weeks, they gave these mice a mix of antibiotics through their drinking water before infecting them with the flu virus. They also infected some mice that they had not treated with the antibiotic mix so that they could compare the outcomes.
The team noticed that approximately 80 percent of the untreated mice with healthy gut bacteria survived the infection with the flu virus. Yet, of the mice who had previously received the antibiotic mix, only one-third were able to survive the viral infection.
Inappropriate use of antibiotics not only promotes antibiotic resistance and kills helpful gut bacteria, but may also leave us more vulnerable to viruses.
This could be relevant not only in humans but also livestock animals, as many farms around the world use antibiotics prophylactically. Further research in these environments is urgently needed to see whether this makes them more susceptible to viral infections, said the researchers.
In attempting to find exactly how ingesting antibiotics weaken the mice before their exposure to the flu, the researchers found that type I interferon signaling — a form of protein signaling that regulates the response of a type of cell that lines the lungs — is key to stopping the flu virus from replicating in the lungs.