Abstract

Cigarette smoke exposure is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Our research aims to understand how environmental exposures, particularly cigarette smoke, shape macrophage-mediated immune responses in the lung. We have demonstrated that cigarette smoke profoundly alters macrophage responses to pathogens by suppressing the early inflammatory response while promoting regulated lytic cell death, resulting in the extensive release of damage-associated molecular patterns (DAMPs).

We are currently investigating the mechanisms by which macrophage death drives and amplifies lung inflammation, with the aim of determining whether fine-tuning cell death pathways could provide a novel therapeutic strategy to limit excessive inflammation. We are also exploring the role of the pore-forming gasdermin family proteins in regulating inflammatory cell death and mitochondrial dysfunction. In addition, we study how extracellular vesicles released by dying macrophages contribute to inflammatory signaling and the propagation of immune responses within the lung.

By elucidating the molecular mechanisms linking cigarette smoke exposure, macrophage cell death, and chronic lung inflammation, our research seeks to identify novel therapeutic targets for COPD and other chronic inflammatory lung diseases.

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