Multiple new NIH grants for Markus Bosmann
Congratulations to Markus Bosmann and his team for receiving a new R03 and two new R01 grants over the last few months! So much good news in such a short tome period is remarkable and truly something to celebrate!!!
New R03 will develop new models to study complement receptor signaling (“Generation of C5aR-TurboID mice”)
The complement system is an important component of the innate immune defenses. During infection or tissue injury, complement proteins generate signals that rapidly recruit and activate immune cells. One of the most powerful of these signals is C5a, which acts through two receptors, C5aR1 and C5aR2. Although both receptors have important roles in inflammation and host defense, the molecular networks through which they regulate immune-cell behavior remain incompletely understood.
The new project will generate genetically engineered mouse models that make it possible to track these receptors and identify proteins located in their immediate molecular environment. The approach will use proximity labeling, a technology that can capture receptor-associated protein networks directly within living cells.
Initial studies will focus on macrophages and neutrophils, key immune cells in infection and inflammatory disease. These new models will provide broadly useful tools for defining how C5aR1 and C5aR2 function in health and disease and for investigating complement signaling in future studies of lung inflammation, infection, and tissue injury.
New R01 to investigate immune defense during bacterial sepsis (“PACC1 in host defense against bacterial infections and sepsis“)
Macrophages are critical first-line immune cells that engulf and eliminate invading bacteria. The project will examine how PACC1, a proton-activated ion channel highly expressed in macrophages, supports phagocytic bacterial clearance and immune responses during sepsis and pneumonia.
Using genetic models and advanced immune profiling, the studies aim to better understand mechanisms that enable macrophages to control bacterial infections and protect against severe sepsis.
New R01 to investigate pneumonia (“The Protective Role of GNB2 in Macrophages during Legionella Pneumonia”)
The project will examine how signaling pathways in macrophages control inflammatory responses and elimination of intracellular bacteria, including Legionella. Using genetic models, proteomics, and studies of human macrophages, the work aims to define mechanisms that strengthen innate immune defense in the lung.