We aim to elucidate the biochemical, immunological, and molecular mechanisms that restore organ-specific and systemic homeostasis after pathological challenges, and why these mechanisms occasionally fail, leading to chronic inflammation.
Our research centers in a a key scientific challenge in human pathophysiology: how to harness endogenous resolution mechanisms of inflammation when initial resolution fails. From birth, our bodies are continuously exposed to a myriad of environmental factors, pathogens, and injuries that trigger acute inflammatory responses. These responses are crucial for combating infections, healing wounds, and safeguarding overall health. Ideally, these inflammatory reactions are self-limited, leading to complete resolution of leukocyte infiltration and clearance of cellular debris by macrophages , thereby restoring and maintaining tissue homeostasis. The mechanisms involved in resolution of inflammation are essential for preventing excessive tissue damage, autoimmunity, and progression to chronic inflammation. Without effective resolution mechanisms, our ability to recover from even minor injuries or infections would be severely compromised, leading to serious health issues.
Elucidating the Mechanisms by Which Resolvins Regulate Macrophage Phagocytosis
Lipid Remodeling in Macrophages During Cargo-Specific Phagocytosis
Specialized pro-resolving mediators (SPMs) control neutrophil deployment, infiltration, and phagocytic ability.
Classifying Neutrophil Dynamics via Imaging
Dissecting Neutrophil Heterogenity Via Functional Analysis
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