The focus of our research is to understand multiple aspects of lung biology and inflammatory lung diseases. Broadly, the research employs murine models of pathogens- and toxicant-induced inflammation. Using these models of lung inflammation, the research aims to understand the roles of macrophages in the orchestration of inflammatory responses. Unlike traditional view, emerging evidences suggest macrophage as a highly plastic cell type with likely roles in regulation of initiation, progression and resolution of inflammatory responses. Ongoing research in the laboratory has established several tools to characterize macrophage responses. Currently active projects include, understanding macrophage number maintenance in lung, studying macrophage activation heterogeneity, and understanding roles of macrophages in different murine models of lung inflammation. The ultimate goal of this research is to develop diagnostic biomarker of lung diseases and therapeutic interventions to modulate inflammatory responses. The laboratory uses wide range of in vitro and in vivo models and techniques including confocal microscopy, flow cytometry, clinical biochemistry, immunochemical staining, magnetic-associated cell sorting, cellular and proteomic analyses of biological samples, molecular biology (PCR, RT-PCR, Gene expression analyses etc.) and cytokine assays.

Experimental In Vivo Models
Cystic Fibrosis: The laboratory employs, Scnn1b-Tg mouse, a model of muco-obstructive lung disease that recapitulate human cystic fibrosis lung disease. We have crossed these mice to several other strains to introduce various defects in immune responses. We are focused on understanding how innate, innate lymphoid, and adaptive immune systems interact to shape mucobstructive lung disease in these mice.

Allergic Asthma: We are interested in understanding how myeloid cells, including macrophages and cDCs, orchestrate allergic asthma responses.

Ozone-induced Airway Disease: Our laboratory is investigating how ozone exposures modulate muco-obstructive airway diseases. We have a state-of-the-art ozone exposure facility and lung disease phenotyping facility for rodents.

Second hand smoke (SHS)-induced COPD: We have recently published a manuscript highlighting the effect of early postnatal second hand smoke exposure on the development of muco-obstructive airways disease. Moving forward, we are interested in studying interactions between second hand smoke, airway bacterial clearance, and myeloid cell-mediated immune responses.



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