Exposure to cigarette smoke decreases the effectiveness of the antiviral and antioxidant defenses of the respiratory tract facilitating infection by the rhinoviruses responsible for the common cold.
The epithelial cells that line the respiratory tract represent our first line of defense against the many aggressors present in the external environment, whether fine particles from atmospheric pollution, certain toxic agents (smoke, solvents) or even of several respiratory viruses.
In the case of viruses, it is the approximately 100 distinct species of rhinoviruses responsible for the common cold that pose one of the most common threats: following their entry into the respiratory cells, these viruses multiply rapidly and cause the characteristic symptoms of the common cold. , including runny nose, sneezing, coughing, congestion and headache. Although most of the time they are not very dangerous for health, colds nevertheless cause significant direct and indirect health costs each year.
The respiratory tract naturally defends itself against viruses
The presence of viruses in the respiratory tract is much more common than one might think: for example, a study that continuously measured the presence of respiratory viruses in the nasal passages indicates that an average person is a carrier of these viruses. about 7 weeks per year. On the other hand, despite this very involuntary cohabitation, about half of these infections are totally asymptomatic, which suggests that the respiratory tract has a first-line defense mechanism that significantly reduces the infectious potential of these viruses.
To better understand the mechanisms involved in the defense of the airways against viruses, a team from Yale University (New Haven, Connecticut) exposed cells taken from the nasal passages and bronchi to a common rhinovirus (RV-1B) and subsequently examined the response triggered by the infection. They noticed that the virus activated two types of responses:
1) an antiviral response, characterized by a strong production of type III interferon (a class of proteins which has the function of stimulating the immune system);
2) an antioxidant response, with the expression of several free radical neutralizers. The antiviral response is mainly located in the nose, which is logical since this is the entry point for the virus, while the antioxidant response is mainly present in the lungs, which is also logical because the constant presence of potentially toxic aggressors in the air breathed.
According to the study authors, this specialization of antiviral and antioxidant defenses in distinct places (nose and lung) suggests that the cells of the respiratory tract cannot deploy these two weapons simultaneously and must choose between defending themselves against a virus or protecting themselves. against oxidative stress. This trade-off is well illustrated by the observation that nasal cells exposed to cigarette smoke are highly susceptible to rhinovirus infection. In these cells, the activation of a transcription factor responsible for the antioxidant response (NRF2) causes a series of adaptations intended to promote survival, but is accompanied in parallel by a decrease in the production of interferon and therefore of the antiviral response. In other words, the airways are very good at defending themselves against viruses and other types of airborne toxic aggressors, but become much more susceptible to viral infection when exposed to both attacks simultaneously.
These observations explain why people who are chronically exposed to oxidative stress such as smokers, patients with chronic obstructive pulmonary disease (COPD) or even people with asthma are much more susceptible to the cold virus and more often develop complications from the cold. following the infection.
Fendrick AM et al. The economic burden of non-influenza-related viral respiratory tract infection in the United States. Arch. Intern. Med. 2003; 163: 487-94.
Mihaylova VT et al. Regional differences in airway epithelial cells reveal tradeoff between defense against oxidative stress and defense against rhinovirus. Cell Rep. 2018; 24: 3000-3007.