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Smoking and air pollution affects latent tuberculosis: According to a new study from researchers at the University of Alabama at Birmingham (UAB), a toxic gas present in air pollution and tobacco smoke plays a significant role in triggering tuberculosis infection, This study focused on carbon monoxide (CO), a colorless, odorless gas present in tobacco smoke, and vehicle and manufacturing plant emissions. Also, CO is produced naturally in brushfires and volcanic gas. The study showed that CO triggers Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, to shift from active infection to a drug-resistant dormant state. This is called latency, a global problem that results in tuberculosis escaping detection and treatment, and which contributes to overall tuberculosis transmission. This study gives the first description of a role for CO in mycobacterial pathogenesis, and may explain why smoking and air pollution contributes to TB. In the study, the researchers worked with Mtb cells under biosafe laboratory conditions and found Mtb proteins 'sense' CO at the molecular level, much like the bacteria's proteins sense other gases in the lungs. The CO interaction is what led to a series of biological steps that sent Mtb into latency. The finding has significant political, environmental and social implications for speeding up clean-air measures as a way to improve public health. This study also helps to discover new ways to fight extreme drug-resistant tuberculosis, or XDR TB, the UAB. One third of the world's population is infected with undetectable forms of tuberculosis, which hinders screening and eradication efforts. This finding shows that exposure to high levels of CO through air pollution and cigarette smoke plays a role in tuberculosis infection rates. Also, the study showed that low levels of CO present in the body are capable of triggering tuberculosis latency. Inflammation, infection and oxidative stress are among contributors to CO in the body.
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