Misuse of antibiotics increases the risk of viral infection

July 2, an article published in Cell Reports noted that enhancing the signaling of basic type I interferon (IFN alpha/β) activates cell antiviral responses, inhibits the replication of influenza viruses, and relieves symptoms such as weight loss in mice. However, once treated with antibiotics, the antiviral effects of gut microorganisms are greatly reduced.
study tells us that abusing antibiotics not only increases bacterial resistance and destroys health-beneficial intestinal symbloid microbiota, but also increases the risk of viral infections. Lead author and researcher at the Francis Crick Institute in the UK, Andreas Wack said.
IFN alpha/β signal conduction against viral immune responses is critical, and these path pathraps help the body achieve very clever regulation, stimulating antiviral responses while avoiding inflammatory reactions that damage normal tissue. The antiviral response is a "double-edged sword", which occurs in individuals with higher levels of interferon-producing gene variants: on the one hand, their antiviral immune response is indeed stronger, but on the other hand, they are plagued by chronic autoinflammive responses. IFN alpha/β signaling balances the positive and negative effects of antiviral responses while minimizing the risk of excessive inflammatory response/harm. However, scientists do not yet know its specific regulatory mechanisms.
To study the problem, Wack led the team in introducing mice with higher levels of basic IFN alpha/β signaling, who were more resistant to influenza viruses, lost less weight when they became ill, had lower levels of gene expression eight hours after infection, and were inhibited by flu virus replication two days after infection. The IFN alpha/β signaling path and antiviral immune response in the mice did not "run at full power" because the virus load was controlled in advance in the experiment. Experimental results show that the key to regulating ifN alpha/β conduction of lung cells may lie in regulating the expression level of IFN alpha/β receptors.
after two to four weeks of antibiotic treatment, the mice did not perform as well as they would have liked against the flu virus. Antibiotic therapy reduces IFN alpha/β signaling levels in pulmonary β cells, thereby weakening the immunity of IFN alpha/β path path. However, after receiving a fecal transplant, the damage caused by antibiotics to the immunity of mice was reversed, proving that gut microbes may have played a role.
results showed that the gut microbiome in mice increased IFN alpha/β signal conduction levels in lung substation cells, thus increasing the mice's resistance to influenza viruses. The new findings in this study also support the findings of previous studies that mice treated with oral antibiotics were more susceptible to a variety of viruses, including influenza A virus.
Wack team hopes to further determine in future studies where the microbiome is promoting antiviral response and what its specific mechanisms are. (Source: Zhang Siwei, China Science Journal)
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