We investigate how neutrophils make decisions in living organisms and how systemic context reshapes those decisions over time. Across injury, metabolic imbalance, aging, trauma, and chronic inflammatory states, we study how neutrophils integrate competing signals to drive coordinated immune programs. This allows us to define how inflammation favors repair, adaptation, or dysfunction—and ultimately shapes long-term biological outcomes.
All of our projects are unified by this logic:
Context → Immune Decisions → Coordinated Programs → Outcomes
Below are the major themes where we apply and develop this framework.
Our work shows that immune responses are not fixed reactions but context-dependent behaviors. We study how metabolic state (metainflammation), aging (inflammaging), and environmental stress systematically reshape neutrophil behavior long before disease appears.
Metabolic challenges reprogram neutrophil migration and function.
Aging alters signaling responses.
Chronic stressors change innate immune trajectories.
These studies reveal that context is not backdrop — it is instruction.
Neutrophils operate as integral components of whole-organism networks. Using real-time approaches, we observe how they integrate signals from multiple tissues and competing injuries.
Neutrophil prioritization is an active choice, not random.
Signal integration alters response hierarchy.
Decision timing predicts organism-level outcomes.
This theme demonstrates that understanding immune biology requires living, systemic observation, not static snapshots.
Rather than isolated gene lists, we define immune programs — coordinated networks of expression, signaling, and behavior that reflect system state. We use dynamic imaging and high-dimensional analysis to characterize:
adaptive vs maladaptive programs.
trajectories that lead to repair or dysfunction.
how cues from organ contexts influence neutrophil states.
This area connects behavior to molecular and cellular identity without losing the organism-level picture.
Mechanistically informed discovery is only useful if it informs human health. We integrate in vivo findings with:
primary human neutrophil studies.
patient cohort data.
multiomic analyses.
This translation anchors our work in disease relevance and opens paths to biomarkers and intervention logic that respect timing and context.
"Neutrophil Tornado" - by Cassia Michael
Zebrafish xenograft showing neutrophil response (in cyan) to Anaplastic Thyroid cancer cells (magenta).
We develop and use platforms that integrate:
long-term intravital imaging.
genetic and perturbation tools.
scalable, longitudinal assays.
computational and systems analysis.
These platforms are not ends in themselves — they are how we measure decision processes that were previously invisible.
"Neutrophil Attack" - by Juliana Gomes
Neutrophils can be reprogramed into anti cancer phenotypes. Intravital microscopy video showing neutrophils (Green) attacking and clearing liver cancer cells (Red) transplanted into a zebrafish larvae after drug treatment targeting a key molecular pathway that regulated neutrophil infiltration and function.
Tumors hijack neutrophils. We study how to take them back.
By integrating human cancer genomics with zebrafish genetic and xenotransplant models, we visualize neutrophil behavior in real time. Through long-term intravital imaging and functional profiling, we identify novel pathways that reprogram neutrophils into powerful anti-cancer effectors.
Science you can see. Immunity you can redirect.