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Recent research published in science journal has shed light on the intensified risk of active tuberculosis (TB) among tobacco smokers, with smoking accounting for up to 20% of global TB cases. The mechanisms through which smoking fosters lung conditions conducive to Mycobacterium tuberculosis (Mtb) growth have remained elusive.
Through extensive investigations utilizing single-cell RNA sequencing (scRNA-seq), flow cytometry, and functional assays on primary bronchoalveolar lavage cells, scientists delved into understanding the impact of smoking on lung microenvironments. A notable finding was the prevalence of immature inflammatory monocytes in the lungs of smokers compared to nonsmokers. These monocytes displayed traits indicative of recent recruitment from the bloodstream, ongoing differentiation, heightened activation, and characteristics akin to chronic obstructive pulmonary disease.
The research also pinpointed CD93 as a distinguishing marker for a specific subset of these newly recruited smoking-associated lung monocytes. Moreover, the study revealed that the recruitment of these cells into the lungs was facilitated by chemokines binding to CCR2, including CCL11. Importantly, these cells exhibited elevated inflammatory reactions upon encountering Mtb, promoting accelerated growth of the pathogen within the cells. However, the study found that anti-inflammatory compounds could impede this heightened Mtb growth, establishing a link between smoking-induced pro-inflammatory states and increased susceptibility to Mtb.
The findings propose a model wherein smoking triggers the migration of immature inflammatory monocytes from the bloodstream into the lungs, fostering the accumulation of these cells conducive to Mtb growth in the airways. This research not only delineates how smoking heightens vulnerability to Mtb but also identifies potential host-directed therapies to alleviate the burden of TB among smokers.
