Runny nose, sneezing, throat scratching: the classic cold has probably caught everyone once before. Responsible for this annoying suffering can be a variety of viruses – especially representatives of the so-called rhinoviruses. If the pathogens infect our airways, they sometimes cause unpleasant and in extreme cases even severe symptoms of disease. In many cases, our immune system will kill the pathogens before we notice anything about the infection.
But why do the cold viruses regularly bring people out of action, while others almost never get sick? Scientists led by Valia Mihaylova of Yale University, New Haven, have now studied how such different disease histories can be explained.
Attack on the airways
For their research, they examined epithelial cells from the nasal cavity and the lungs of healthy people. These cells form the first line of defense of the body against potentially dangerous invaders in the air. How do they react when they come into contact with rhinoviruses? It revealed that although both cell types were exposed to identical conditions in the experiment, they did not exhibit the same behavior.
For example, the researchers observed a much stronger antiviral response in the cells of the nose – this is also where the pathogens typically begin their airway conquest. However, further studies have shown that nasal and lung cells apparently set different priorities for a rhinovirus infection. Although the antiviral response in the nose had increased, the cells in the lungs could effectively prevent oxidative stress. This type of cell stress can be caused by viruses, but also by cigarette smoke or pollen.
But why do not both cell types rely equally on both antiviral and antioxidant strategies? Apparently, because they have to choose one of them. As the scientists pointed out, the immune response to oxidative stress largely eliminates antiviral defense mechanisms.
To further investigate this relationship, the team passed on the nasal cells with cigarette smoke – and caused oxidative stress – and immediately infected them with rhinoviruses. The result: in comparison with the first experiment, the cells have significantly worsened the virus attack. "Although they survived the cigarette smoke, they could not effectively fight the pathogen," says Ellen Foxman, Mihaylova's colleague.
These results underline how sensitive the balance is between the various defense mechanisms of our body – and that cells, depending on their place of origin, set each other's priorities in the defense. Certain environmental influences can shift the customized immune response in one direction or the other, but this involves costs.
"The respiratory system protects us against pathogens and other harmful substances and they do well as long as they have to deal with just one stressor, but with two stressors they have to compromise at the same time," says Foxman. "They can adapt to a different type of stress, but pay for it with greater susceptibility to other harmful influences – such as rhinoviruses."
Smokers are more sensitive
It seems that there is a link between certain environmental influences and the risk of colds by the individual. According to the researchers, this can also explain why smokers are often more susceptible to rhinovirus infections and are more susceptible to colds and cooperatives than non-smokers. (Cell Reports, 2018; doi: 10.1016 / j.celrep.2018.08.033)
This article was written by DAL