Air pollution, smoking play role in triggering latent tuberculosis

Washington, May 14 : Researchers at the University of Alabama at Birmingham (UAB) have found that a toxic gas present in air pollution and tobacco smoke plays a significant role in triggering tuberculosis infection.

For the study, researchers study focused on carbon monoxide (CO), a colourless, odourless gas present in tobacco smoke, and vehicle and manufacturing plant emissions.

CO is also produced naturally in brushfires and volcanic gas.

In the study, researchers 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 is the first description of a role for CO in mycobacterial pathogenesis, and may explain why smoking and air pollution contributes to TB," said Adrie Steyn, Ph.D., assistant professor in UAB's Department of Microbiology and lead author on the study. uring 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.

According to researchers, the finding holds political and social implications for speeding up clean-air measures as a way to improve public health, in addition to the environmental significance.

They said that the study holds promise for helping to discover new ways to fight extreme drug-resistant tuberculosis, or XDR TB.

"We're talking about huge socio-economic and public health implications," Steyn said.

The finding contributes to a growing understanding that exposure to high levels of CO through air pollution and cigarette smoke plays a role in tuberculosis infection rates.

Besides this, 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.

The findings were published online in The Journal of Biological Chemistry.

ANI