Reactive oxygen species elevations in human immune cell subsets during sepsis are mitigated by norepinephrine and N-acetylcysteine

doi:10.5492/wjccm.v14.i4.108638

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 14, Issue 4

This Article

Peer-Review Report of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (941)

All Articles published online

The chart showing PDF series, HTML series, Figures (1-4) series.

Item

Count

PDF

HTML

164

Figures (1-4)

Sum=217

Featured Article

The chart showing Browse series, Download series.

Item

Count

Browse

101

Download

295

Sum=396

Publishing Process of This Article

Item

Count

Browse

Download

219

Sum=283

Dec 9, 2025 (publication date) through Feb 16, 2026

Times Cited of This Article

Times Cited (0)

Journal Information of This Article

Publication Name

World Journal of Critical Care Medicine

ISSN

2220-3141

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Study

World J Crit Care Med. Dec 9, 2025; 14(4): 108638
Published online Dec 9, 2025. doi: 10.5492/wjccm.v14.i4.108638

Reactive oxygen species elevations in human immune cell subsets during sepsis are mitigated by norepinephrine and N-acetylcysteine

Joby Thoppil, J David Farrar, Drashya Sharma, Shaun Kirby, Angela Mobley, Daniel Mark Courtney

Joby Thoppil, Daniel Mark Courtney, Department of Emergency Medicine, The University of Texas Southwestern Medical Center, Dallas, TX 75390, United States

J David Farrar, Drashya Sharma, Shaun Kirby, Angela Mobley, Department of Immunology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, United States

Author contributions: Thoppil J contributed to experimental design, performance, analysis and manuscript preparation; Farrar JD contributed to experimental design, analysis and manuscript preparation; Sharma D, Kirby S, and Mobley A all contributed to experimental performance and manuscript preparation; Courtney DM contributed to manuscript preparation; all the authors read and approved the final version of the manuscript to be published.

Supported by Emergency Medicine Foundation; and Zoll Foundation.

Institutional review board statement: This work was approved by the Institutional Review Board at the University of Texas Southwestern Medical Center.

Conflict-of-interest statement: The authors have no conflict of interest statement.

Data sharing statement: No additional data are available.

Corresponding author: Joby Thoppil, MD, PhD, Assistant Professor, Department of Emergency Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd E6.110A, Dallas, TX 75390, United States. joby.thoppil@utsouthwestern.edu

Received: April 20, 2025
Revised: May 13, 2025
Accepted: May 29, 2025
Published online: December 9, 2025
Processing time: 223 Days and 18.2 Hours

Core Tip

Core Tip: Sepsis is a life-threatening condition characterized by immune dysregulation, in which peripheral blood mononuclear cells are believed to play a central role. Reactive oxygen species (ROS) are critical to immune cell signaling, but excessive ROS may contribute to immune alterations during sepsis. In this observational study, we demonstrate elevated ROS levels in CD3+ T cells and CD14+ monocytes from septic patients. Using in vitro models, we show that norepinephrine and N-acetylcysteine attenuate ROS accumulation following inflammatory stimulation. These findings suggest that targeting oxidative imbalance may represent a promising direction for future sepsis research.