Is this project an undergraduate, graduate, or faculty project?

Undergraduate

Project Type

group

Campus

Daytona Beach

Authors' Class Standing

Graeme Grainger, Senior

Lead Presenter's Name

Graeme Grainger

Lead Presenter's College

DB College of Arts and Sciences

Faculty Mentor Name

Dr. Amber Paul

Abstract

Long-duration spaceflight exposes astronauts to chronic ionizing radiation and microgravity that disrupts homeostasis in the immune system and cellular metabolism. While simulated spaceflight models demonstrate altered T-cell polarization and sex-dependent shifts toward regulatory phenotypes, the metabolic mechanisms driving these immune changes remain unclear. Immune cell function is tightly linked to metabolic programming, with effector T cells relying on glycolysis and regulatory T cells favoring oxidative metabolism, making them highly sensitive to shifts in nutrient availability and redox balance. Emerging research further suggests that neutrophils act as metabolic regulators capable of reshaping the immune microenvironment through oxidative stress, cytokine production, and nutrient competition, thereby influencing T-cell differentiation. This project will investigate how simulated microgravity combined with 5-ion galactic cosmic radiation alters systemic metabolic markers (glucose, lactate, hematocrit), neutrophil activation states, and T-cell subsets (FoxP3⁺ Tregs, IFNγ⁺ Th1, cytotoxic T cells) using flow cytometric and correlation analyses. By integrating metabolic profiling with innate and adaptive immune phenotyping, this study aims to define how spaceflight-associated metabolic disruption drives immune dysregulation and to identify mechanistic targets for preserving astronaut immune resilience during long-duration missions beyond low Earth orbit.

Did this research project receive funding support (Spark, SURF, Research Abroad, Student Internal Grants, Collaborative, Climbing, or Ignite Grants) from the Office of Undergraduate Research?

No

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Metabolic Regulation and Immunity in the Spaceflight Environment

Long-duration spaceflight exposes astronauts to chronic ionizing radiation and microgravity that disrupts homeostasis in the immune system and cellular metabolism. While simulated spaceflight models demonstrate altered T-cell polarization and sex-dependent shifts toward regulatory phenotypes, the metabolic mechanisms driving these immune changes remain unclear. Immune cell function is tightly linked to metabolic programming, with effector T cells relying on glycolysis and regulatory T cells favoring oxidative metabolism, making them highly sensitive to shifts in nutrient availability and redox balance. Emerging research further suggests that neutrophils act as metabolic regulators capable of reshaping the immune microenvironment through oxidative stress, cytokine production, and nutrient competition, thereby influencing T-cell differentiation. This project will investigate how simulated microgravity combined with 5-ion galactic cosmic radiation alters systemic metabolic markers (glucose, lactate, hematocrit), neutrophil activation states, and T-cell subsets (FoxP3⁺ Tregs, IFNγ⁺ Th1, cytotoxic T cells) using flow cytometric and correlation analyses. By integrating metabolic profiling with innate and adaptive immune phenotyping, this study aims to define how spaceflight-associated metabolic disruption drives immune dysregulation and to identify mechanistic targets for preserving astronaut immune resilience during long-duration missions beyond low Earth orbit.

 

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