Research Area 

Despite unprecedented progress in biomedical science, pneumonia remains the leading cause of death worldwide.  Pneumonia leads to Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS), critical conditions associated with high mortality due to uncontrolled inflammatory response. Although Inflammation is necessary to clear invading pathogens, if unchecked, it leads to collateral tissue damage and compromises lung function. Moreover, the initial hyper-inflammatory phase in these diseases is followed by an immunosuppressive stage, which predisposes patients to secondary infections. Disproportionate cell death during ALI/ARDS leads to the release of Damage Associated Patterns (DAMPs). Cardiolipin (CL) is one such DAMPs of mitochondrial origin.  Our research has shown that CL blocks lung inflammation resolution by inhibiting IL-10 production, suggesting an immunomodulatory role of CL linked with ALI pathophysiology. We aim to understand the effect of mitochondrial DAMPs on the severity of ALI by studying both the early and late phases of the disease. Our approach combines basic research, animal models, and patient samples to translate the findings into effective therapeutics.

Klebsiella pneumoniae (KP) is one of the primary etiological agents in hospital-acquired pneumonia. Pneumonia caused by KP often leads to bacteremia in critically ill patients and is associated with high mortality. The recent emergence of the Carbapenem-resistant strain worsened the situation by severely limiting treatment options. In such precarious circumstances, boosting the host immune response might be the last resource to reduce mortality. In a parallel study, we investigate how the host immune system, particularly the innate immune response, functions against carbapenem-resistant KP. Using patient samples and immune cells enriched from human volunteers, we employ high-throughput transcriptome analysis and several state-of-the-art molecular biology and immunology tools to investigate the immune response against KP.