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Zinc accelerates respiratory burst termination in human PMN
Annika Droste1, Gustavo Chaves2, Stefan Stein3
1Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, Nuremberg, Germany; Department of Gynecology and Obstetrics, Johannes Gutenberg University, Mainz, Germany.
Redox Biology
|September 25, 2021
Summary
Phagocyte respiratory burst relies on NADPH oxidase (NOX2) and voltage-gated proton channels (Hv1). This study reveals their essential interconnection and how zinc terminates this crucial immune response.
Area of Science:
- Immunology
- Cell Biology
- Biophysics
Background:
- Phagocyte respiratory burst is vital for innate immunity, utilizing reactive oxygen species (ROS) produced by NADPH oxidase (NOX2).
- NOX2 activity involves electron translocation and proton release, impacting cellular charge and pH.
- Voltage-gated proton channels (Hv1) play a role in regulating these cellular changes.
Purpose of the Study:
- To investigate the interplay between NOX2 and Hv1 during the phagocyte respiratory burst.
- To compare ROS production in primary human polymorphonuclear leukocytes (PMN) and the PLB 985 cell line.
- To explore the role of zinc in regulating the respiratory burst.
Main Methods:
- Recording ROS production in PMN and PLB 985 cells while inhibiting Hv1.
- Developing a mathematical model based on NOX2 and Hv1 biophysical properties.
- Utilizing flow cytometry to assess cell viability under different conditions, including zinc chelation.
Main Results:
- Human PMN and PLB 985 cells exhibit a conserved ROS production mechanism involving NOX2 and Hv1.
- A mathematical model supports the interconnected function of NOX2 and Hv1.
- Zinc chelation was found to irreversibly terminate the respiratory burst, with high zinc concentrations inducing cell death.
Conclusions:
- Hv1 and NOX2 are essentially interconnected in the phagocyte respiratory burst.
- Zinc plays a critical role in the termination of this immune response.
- Understanding these interactions can elucidate complex protein dynamics and immune response regulation.
