Commensal Bacteria Fight Viral Infections
The bacterial communities that live in healthy humans are essential to the process of fighting off viral infections, according to a new study from the Perelman School of Medicine, University of Pennsylvania.
There is an enormous diversity of bacteria and other microbes that live in a healthy human. These microbes help us in many ways, from the digestion of food to a strong immune system. And according to this new research, without them we wouldn’t be able to fight off viral infections.
“From our studies in mice, we found that signals derived from these beneficial microbes are essential for optimal immune responses to experimental viral infections,” says David Artis, an associate professor of microbiology. “In one way we could consider these microbes as our ‘brothers in arms’ in the fight against infectious diseases.”
These commensal bacteria influence our immune-cell development and our susceptibility to infectious or inflammatory disease. The surfaces of the skin, vaginal, upper respiratory, and gastrointestinal tracts of mammals are colonized by these microbial communities, and consist of bacteria, fungi, protozoa, and viruses. The communities living in the intestines are the largest and most diverse of these.
Studies have previously shown that patients with alterations in their bacterial communities are more susceptible to diabetes, cancer, obesity, allergies, inflammatory bowel disease, and other disorders. Even though we’ve known all of this for awhile, how commensal bacteria actually regulates immunity after we are exposed to pathogens is not yet understood.
So, to learn more about this, the researchers explored several different, complementary lines of investigation. The researchers first showed that mice that have been treated with antibiotics to intentionally reduce their numbers of commensal bacteria show an “impaired antiviral immune response and a substantially delayed clearance of a systemic virus or influenza virus that infects the airways.”
More interestingly, the mice that have been given antibiotics, “had severely damaged airways and increased rate of death after the experimental influenza virus infection, demonstrating that alterations in commensal bacterial communities can have a negative impact on immunity against viruses.”
The researchers then profiled the genes that were expressed in immune cells that are called macrophages, isolated from the antibiotic-treated mice. The data showed a decreased expression of the genes that are associated with antiviral immunity.
Also, macrophages from antibiotic-treated mice showed “defective responses to interferons, proteins made and released in response to viruses, bacteria, parasites, or tumor cells.” Normally, interferons facilitate communication between different cells in order to trigger the immune cells that then attack the pathogens or tumors. The mice treated with antibiotics also had a damaged capacity to limit the replication of the virus. Though, if the mice were treated with a compound that then restored interferon responsiveness, protective antiviral immunity was re-established.
“It is remarkable that signals derived from one type of microbe, in this case bacteria, can have such a profound effect on immune responses to viruses that are a very different type of microbe,” says first author Abt. “Just like we would set a thermostat to regulate when a heater should come on, our studies indicate that signals derived from commensal bacteria are required to set the activation threshold of the immune system.”
These lines of evidence, when taken together, show that signals from commensal bacteria stimulate immune cells in a way that is optimal for our antiviral immunity.
“Although more work needs to be done, these findings could illuminate new ways to promote better immunity to potentially life-threatening viral infections,” adds Artis.
Source: Perelman School of Medicine at University of Pennsylvania
Image Credits: Meera Nair, PhD, Michael Abt, PhD, and David Artis, PhD, Perelman School of Medicine, University of Pennsylvania; Gregory Sonnenberg, Ph.D.; David Artis, Ph.D., Perelman School of Medicine University of Pennsylvania; Science