Bradley E. Hiller

This study identifies Oncostatin M (OSM) as a critical regulator of pulmonary host responses during influenza and bacterial pneumonia, revealing non-canonical signaling pathways.

The paper defines sub-phenotypes of pneumonia using histopathological features from human lung samples and validates them in mouse models.

The paper shows that neutrophils in a murine pneumococcal pneumonia model transition through two distinct transcriptional trajectories with associated metabolic changes.