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Sitagliptin Modulates Functional and Phenotypic Properties of Human Neutrophils Under Normal- and High-Glucose
Vanja Mališ1, Marija Drakul1, Sara Rakočević1
1Faculty of Medicine Foča, University of East Sarajevo, Studentska 5, 73300 Foča, Bosnia and Herzegovina.
Molecules (Basel, Switzerland)
|May 4, 2026
Summary
Sitagliptin, a type 2 diabetes drug, reduces inflammation by decreasing reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in neutrophils. It also alters neutrophil surface markers, suggesting an anti-inflammatory and immunomodulatory effect.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Sitagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor for type 2 diabetes.
- Emerging evidence suggests sitagliptin possesses anti-inflammatory and immunomodulatory properties.
- Human neutrophils play a role in inflammation and immune responses.
Purpose of the Study:
- To investigate sitagliptin's effects on human neutrophil function and phenotype.
- To assess these effects under normal and high-glucose conditions in vitro.
- To explore sitagliptin's potential as an anti-inflammatory agent beyond diabetes treatment.
Main Methods:
- Human neutrophils were pretreated with sitagliptin and stimulated with various agents (PMA, fMLP, CaI, OpZym).
- Assessed neutrophil survival, reactive oxygen species (ROS) production, and neutrophil extracellular trap (NET) formation.
- Analyzed surface marker expression using flow cytometry.
Main Results:
- Sitagliptin was non-cytotoxic to neutrophils.
- It significantly reduced ROS production and NET formation, particularly under high-glucose conditions.
- Sitagliptin modulated surface marker expression, indicating a less-activated neutrophil phenotype.
- Demonstrated ROS-scavenging activity in a cell-free system.
Conclusions:
- Sitagliptin exhibits potent antioxidative and ROS-scavenging activity in neutrophils.
- It induces a phenotypic shift in neutrophils, suppressing NETosis.
- These findings suggest neutrophils are a cellular target contributing to sitagliptin's anti-inflammatory profile.
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