From granulomas to nanomotors: Active surveillance and microenvironment mapping in the post-tuberculosis Lung.

Microbiological cure of tuberculosis (TB) does not restore normal lung health. Roughly half of TB survivors develop post-tuberculosis lung disease (PTLD), characterized by fibrosis, cavitation, bronchiectasis, and chronic inflammation, and lung cancers frequently arise in or near residual TB scars. This oncogenic risk is under-recognized, and post-TB surveillance remains largely passive, relying on static imaging and low-sensitivity biomarkers that perform poorly in structurally complex lungs. We argue that the central limitation of current surveillance is a mismatch between a dynamic, spatially heterogeneous pathology and inherently static diagnostic tools. Synthesizing clinical and mechanistic evidence, we describe how the post-TB lung is reshaped along three converging axes, namely structural remodeling, immune dysfunction, and metabolic stress, that together recapitulate features of the tumor microenvironment. We then examine nanomotors, a class of self-propelled diagnostic agents able to navigate complex biological media, overcome diffusion and sampling limits, and functionally map high-risk niches. Prioritizing translational feasibility, we focus on near-term applications such as ex vivo biomarker enrichment in sputum and bronchoalveolar lavage fluid, and we place more speculative sensing and therapeutic uses on a staged roadmap. This framework reframes the post-TB lung as an active scar and outlines a biologically aligned strategy for earlier cancer detection and risk-modifying intervention in TB survivors.