Mycobacterium tuberculosis is one of the most successful pathogens in human history and remains a global health challenge. In recent years, a number of lifestyle-related factors have been reported to be associated with tuberculosis (TB). In addition to the role of smoking in cancer initiation and promotion, cigarette smoking is a major risk driving the TB epidemic. Nearly 80% of the world’s 1 billion smokers live in countries of high TB prevalence.
Epidemiologic data have demonstrated that cigarette smokers are more easily infected and have a poor treatment outcome. Compared with non-smokers, smokers have almost twice the risk of TB progression from latent to active disease. Thus, cigarette smokers have impair pulmonary immunity and are more susceptible to lung infections in general.
Mycobacteria infection occurs when inhaled live bacteria reach the alveoli (lower tract of the respiratory system) and successfully evade the initial line of host defense. Tobacco smoke increases the incidence of infection by causing mechanical disruption of cilia function in the airways, thereby permitting an easier pathway for M. tb to reach the alveoli following inhalation of droplets containing bacilli.
In the alveoli, alveolar macrophages are essential for clearing bacteria from the alveolar surface and preventing bacteria-induced infection. While smoking is associated with increased levels of alveolar macrophages, however it has been demonstrated that these cells have defects in controlling M. tb infection. Similar observations have been reported in ex-smokers with persistent immune impairment.
The persistence of cell defect after smoking cessation indicates long-term dampening of protective immunity during M. tb infection in humans. The inability of alveolar macrophage from a smoker to eliminate M. tb infection is linked to impair pro-inflammatory response required for M. tb control.
Also, the impact of cigarette smoke on cell metabolism and function has been explored. Following infection with M. tb, normal human macrophages shift their metabolism towards glycolytic phenotype, which is critical for host defense against infection. However, recent evidence demonstrates fundamental defects in the alveolar macrophages glycolytic response to infection following exposure to cigarette smoke.
This suggests that suppressed pro-inflammatory response reported in smokers may be related to impair macrophages glycolytic response. In addition, alveolar macrophages from the smoker’s lung induce activation of suppressive T-cells, which dampen host immune response.
A smoker’s lung is therefore more immunosuppressed and exhausted than that of non-smokers, resulting in poor response to infections. In summary, there is enough evidence to conclude that smoking is causally associated with active tuberculosis. Thus, patients with TB need and should receive cessation counselling to reduce TB-related mortality.
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