Speaker — Sofia de Oliveira, Albert Einstein College of Medicine assistant professor in the departments of Developmental and Molecular Biology and Medicine (Hepatology)

Title — “Neutrophils on overdrive: How metabolic syndrome hacks immune responses in a zebrafish model”

Abstract — Neutrophils are highly reactive first-line responders that play a central role in detecting threats and orchestrating the entire inflammatory response. They are not only crucial for initiating inflammation but also for resolving it, ensuring proper tissue repair and the restoration of homeostasis. Neutrophils can contribute to both protective and harmful outcomes in a wide range of inflammatory and infectious diseases. Impaired neutrophil function is a key factor not only in increased susceptibility to bacterial infections and mortality but also in poor wound healing and impaired tissue regeneration, particularly in high-risk groups such as patients with metabolic disorders (e.g., diabetes, obesity, metabolic syndrome).

Metainflammation, the chronic low-grade inflammation associated with metabolic disorders, further weakens immune function, making these patients more vulnerable to ongoing inflammation, infections, impaired wound healing, and increased risk of death. Targeting specific neutrophil phenotypes to mitigate their pathogenic effects while enhancing their protective roles represents a promising therapeutic strategy.

However, understanding how metainflammation affects neutrophil biology has been challenging due to conflicting findings in the literature. To address this complexity, a whole-animal approach is crucial for unraveling the intricate cellular and molecular networks influenced by metainflammation, which span multiple organs and tissues. Our lab is addressing this challenge by utilizing zebrafish as a model system. The transparency of zebrafish and the availability of fluorescent reporter lines provide a unique advantage, allowing real-time, non-invasive tracking of neutrophil behavior across different tissues and organs.

We are investigating how metainflammation influences neutrophil production, function, and behavior in both steady-state conditions and in response to injury, infection, or malignancy. Additionally, we explore how these alterations in neutrophil biology impact disease outcomes and how they can be modulated to improve adverse complications and poor prognoses in high-risk groups.

Host — Clyde Campbell, assistant professor in genetics, development and cell biology; and Raquel Espin Palazon, GDCB assistant professor