动物造模,肠道微生物 z-bo 2020-09-11 345

　　Recently, researchers recently published an article in Cell Reports (Celleports) that gut microbes stimulate antiviral signals in non-immune lung cells to protect them from influenza viruses in the early stages of infection. The enhanced baseline type I interferon (IFNα/β) signal promoted antiviral response and reduced mouse influenza virus replication and weight loss, but this protective effect was weakened by antibiotic treatment.

　　"This research supports the view that inappropriate use of antibiotics will not only increase the resistance of antibiotics and eliminate useful defensive probiotics, but also make them vulnerable to viral infections: The corresponding author of the study, Andreas Wacker ( Andreas Wack) said: "It may be so. "In some countries, the livestock industry uses many antibiotics to prevent infection, so treated animals may be more susceptible to viral infections. "

　　IFNα/β signal transmission plays a central role in the immune defense against viral infections. These methods can be fine-tuned to prevent viruses while avoiding tissue damage and inflammation. This balance is evident in individuals with genetic mutations that cause high interferon production. Although they can enhance the immune response to viruses, they show signs of chronic self-inflammation. How IFNα/β signaling regulates this balance to ensure minimal inflammation and maximum antiviral protection remains to be seen. To solve this problem, Wack and his team used mice that increased IFNα/β receptor expression through mutations and increased baseline IFNα/β signaling. These mice are more resistant to influenza virus infection, lose weight, reduce viral gene expression 8 hours after infection, and reduce influenza virus replication after 2 days. The subsequent IFNα/β signal and antiviral immune response were not fully initiated due to early control of virus levels. The results show that regulating the expression level of IFNα/β receptors can accurately regulate the IFNα/β signal in the lung. 2-4 weeks after antibiotic treatment, the protective effect of baseline IFNα/β signal enhancement decreases. The IFNα/β signal of interstitial cells (a group of non-immune cells that make up structural tissues and organs) is mainly reduced. In contrast, fecal transplantation reversed the susceptibility to antibiotic-induced influenza virus infection, suggesting that gut microbes may play a role. Generally, the results show that the flora increases the IFNα/β signal in lung stromal cells, thereby enhancing their ability to resist influenza virus infection. This new finding is consistent with the results of previous studies, which showed that mice treated with oral antibiotics are susceptible to viruses including influenza A.

　　Wack: "In this study and previous studies, microbial signaling works at multiple levels to induce antiviral status in non-immune cells and control infection in the early and late stages of infection. It has been proven to enhance immunity. Force. Cell function."

　　Next, researchers will further study the exact source and mechanism of antiviral resistance caused by microorganisms. Wick said: "Previous studies have shown that microbial-driven signals in lung stromal cells may come from the intestine or lung." However, in the study presented here, the results of stool transplant experiments strongly suggest that the intestine is involved in this effect. I want to know the exact nature of the signal from the intestine to the lungs, and I am studying several hypotheses. "