The Lung Mechanobiology Lab investigates how the mechanical microenvironment of the lung changes with age through extracellular-matrix stiffening, altered alveolar geometry, and loss of tissue compliance and how these mechanical shifts shape the cellular response to inhaled pollutants such as PM2.5. We study how this mechano-axis drives age-associated lung diseases including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and other forms of chronic pulmonary dysfunction. To dissect this biology with physiological fidelity, we engineer in vitro alveolar models that recapitulate the stiffness, geometry, and cyclic mechanics of the in vivo human alveolus across young, aged, and diseased states. These engineered alveoli serve as discovery platforms for mapping mechanobiological checkpoints and as small-molecule drug-screening pipelines aimed at identifying compounds that can reprogramme aged, damaged lung tissue back toward a youthful, repair-competent state.

Project 1: Mechanobiology of the Aging Lung in Air-Pollutant-Induced Dysfunction Aging stiffens lung tissue and amplifies the damage caused by inhaled pollutants such as PM2.5. We build in vitro aged-lung models to map how the mechanical microenvironment shapes the epithelial response to particulate matter, and screen for compounds that can protect older lungs from pollutant-driven dysfunction. (Funded by BITS Pilani)

Project 2: Age-Related Tissue Mechanics in COPD and IPF Development PM2.5 air pollution drives both COPD and IPF, yet the same particle can push aging lungs in opposite directions. Combining engineered alveolar models with PM2.5 sampled across Indian regions, we uncover how age-related stiffness steers the epithelial response  and identify mechanoregulatory targets that can redirect disease trajectory. (Funded by ANRF)

Project 3: Mechanical Regulation of Aged Alveolar Macrophage Function Aged alveolar macrophages lose efficiency at clearing pollutants and pathogens partly because the lung tissue around them stiffens with age. Using engineered aging-mimic substrates, we dissect how mechanical cues regulate macrophage function and search for interventions that restore immune efficiency in the aging lung. (Funded by DST Indo-Italy Joint Research Grant)