The impact of hypoxic conditions on apoptosis and Toll-like receptor 4 expression in polymorphonuclear neutrophils
- Authors
- Kim, Jung-Youn; Choi, Sung-Hyuk; Cho, Young-Duck; Yoon, Young-Hoon; Park, Jong-Hak; Lim, Chae-Seung
- Issue Date
- Jan-2018
- Publisher
- SAGE PUBLICATIONS INC
- Keywords
- apoptosis; hyperoxia; hypoxia; inflammation; neutrophils
- Citation
- EUROPEAN JOURNAL OF INFLAMMATION, v.16
- Indexed
- SCIE
SCOPUS
- Journal Title
- EUROPEAN JOURNAL OF INFLAMMATION
- Volume
- 16
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3947
- DOI
- 10.1177/1721727X18756759
- ISSN
- 1721-727X
2058-7392
- Abstract
- Many patients are admitted to the emergency department due to trauma. Trauma patients suffer from hypoxia due to massive hemorrhage, respiratory failure, and hypovolemic shock. Further damage is caused by reduced immune function and over-expression of inflammatory response. We conducted an experiment to determine the effects of hyperoxia and hypoxia on apoptosis and expression of Toll-like receptor 4 (TLR4) in polymorphonuclear neutrophils (PMNs). Initially, the PMNs were placed in normoxic and hypoxic conditions, and these PMNs were divided into two groups as stimulated or not stimulated with lipopolysaccharide (LPS). Levels of apoptosis and TLR4 expression were measured under normoxic, hypoxic, and hyperoxic conditions. Apoptosis decreased in the hypoxic group than in the normoxic group. With LPS stimulation, apoptosis was decreased in all three treatment groups and even more reduced in the hypoxic group. TLR4 expression increased in all three treatment groups with LPS stimulation, increased further in the hypoxic group, and to a lesser degree in the hyperoxic group. Unlike the cells exposed to hypoxic conditions, the cells exposed to the hyperoxic condition reacted similarly to the cells in the control (normoxic) group. Therefore, the inflammatory reactions can be stronger in the hypoxic group than in the other two groups.
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- Appears in
Collections - 2. Clinical Science > Department of Laboratory Medicine > 1. Journal Articles
- 2. Clinical Science > Department of Emergency Medicine > 1. Journal Articles
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