The inflammatory response of neutrophils in an in vitro model that approximates the postcardiac arrest state

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Abstract

Purpose: Postcardiac arrest syndrome (PCAS) shares many features with sepsis including plasma cytokine elevation with dysregulation of cytokine production, and the presence of endotoxin in plasma. PCAS is closely related to ischemia-reperfusion injury. During ischemia-reperfusion injury, neutrophil, which is the first line of innate immunity, plays a major role. In this study, we investigated the inflammatory response of human neutrophils in an in vitro model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments. Methods: After separation of neutrophils from the whole blood, they were divided into 3 experimental groups: normoxianormoxia, hypoxia-normoxia, and hypoxia-hyperoxia groups. The production of H2O2, the expression of Toll-like receptor 4 (TLR4) receptor, and the extent of apoptosis of the neutrophils were checked. Results: The in vitro hypoxia-normoxia and-hyperoxia models, which simulated the PCAS, showed initiation of the neutrophils' inflammatory reaction by hypoxia insult. Lipopolysaccharide amplifies such inflammation; therefore, prevention of secondary infection may be critical in postresuscitation patients. Temporary hyperoxia following hypoxic insult showed no difference in inflammatory reaction compared with hypoxia-normoxia. Rather, temporary hyperoxia may suppress or minimize inflammation by attenuation of TLR4 receptor. Conclusion: It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100% O2 in a clinical situation may be helpful.

Original languageEnglish
Pages (from-to)217-224
Number of pages8
JournalAnnals of Surgical Treatment and Research
Volume93
Issue number4
DOIs
Publication statusPublished - 2017 Oct 1

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Hyperoxia
Neutrophils
Toll-Like Receptor 4
Reperfusion Injury
Cytokines
Patient Harm
Inflammation
Hypoxia
In Vitro Techniques
Heart Arrest
Coinfection
Innate Immunity
Endotoxins
Lipopolysaccharides
Sepsis
Apoptosis

Keywords

  • Hyperoxia
  • Hypoxia
  • Neutrophil
  • Reperfusion injury

ASJC Scopus subject areas

  • Surgery

Cite this

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title = "The inflammatory response of neutrophils in an in vitro model that approximates the postcardiac arrest state",
abstract = "Purpose: Postcardiac arrest syndrome (PCAS) shares many features with sepsis including plasma cytokine elevation with dysregulation of cytokine production, and the presence of endotoxin in plasma. PCAS is closely related to ischemia-reperfusion injury. During ischemia-reperfusion injury, neutrophil, which is the first line of innate immunity, plays a major role. In this study, we investigated the inflammatory response of human neutrophils in an in vitro model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments. Methods: After separation of neutrophils from the whole blood, they were divided into 3 experimental groups: normoxianormoxia, hypoxia-normoxia, and hypoxia-hyperoxia groups. The production of H2O2, the expression of Toll-like receptor 4 (TLR4) receptor, and the extent of apoptosis of the neutrophils were checked. Results: The in vitro hypoxia-normoxia and-hyperoxia models, which simulated the PCAS, showed initiation of the neutrophils' inflammatory reaction by hypoxia insult. Lipopolysaccharide amplifies such inflammation; therefore, prevention of secondary infection may be critical in postresuscitation patients. Temporary hyperoxia following hypoxic insult showed no difference in inflammatory reaction compared with hypoxia-normoxia. Rather, temporary hyperoxia may suppress or minimize inflammation by attenuation of TLR4 receptor. Conclusion: It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100{\%} O2 in a clinical situation may be helpful.",
keywords = "Hyperoxia, Hypoxia, Neutrophil, Reperfusion injury",
author = "Cho, {Young Duck} and Park, {Sung Jun} and Choi, {Sung Hyuk} and Young-Hoon Yoon and Jung-Youn Kim and Lee, {Sung Woo} and Lim, {Chae Seung}",
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T1 - The inflammatory response of neutrophils in an in vitro model that approximates the postcardiac arrest state

AU - Cho, Young Duck

AU - Park, Sung Jun

AU - Choi, Sung Hyuk

AU - Yoon, Young-Hoon

AU - Kim, Jung-Youn

AU - Lee, Sung Woo

AU - Lim, Chae Seung

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N2 - Purpose: Postcardiac arrest syndrome (PCAS) shares many features with sepsis including plasma cytokine elevation with dysregulation of cytokine production, and the presence of endotoxin in plasma. PCAS is closely related to ischemia-reperfusion injury. During ischemia-reperfusion injury, neutrophil, which is the first line of innate immunity, plays a major role. In this study, we investigated the inflammatory response of human neutrophils in an in vitro model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments. Methods: After separation of neutrophils from the whole blood, they were divided into 3 experimental groups: normoxianormoxia, hypoxia-normoxia, and hypoxia-hyperoxia groups. The production of H2O2, the expression of Toll-like receptor 4 (TLR4) receptor, and the extent of apoptosis of the neutrophils were checked. Results: The in vitro hypoxia-normoxia and-hyperoxia models, which simulated the PCAS, showed initiation of the neutrophils' inflammatory reaction by hypoxia insult. Lipopolysaccharide amplifies such inflammation; therefore, prevention of secondary infection may be critical in postresuscitation patients. Temporary hyperoxia following hypoxic insult showed no difference in inflammatory reaction compared with hypoxia-normoxia. Rather, temporary hyperoxia may suppress or minimize inflammation by attenuation of TLR4 receptor. Conclusion: It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100% O2 in a clinical situation may be helpful.

AB - Purpose: Postcardiac arrest syndrome (PCAS) shares many features with sepsis including plasma cytokine elevation with dysregulation of cytokine production, and the presence of endotoxin in plasma. PCAS is closely related to ischemia-reperfusion injury. During ischemia-reperfusion injury, neutrophil, which is the first line of innate immunity, plays a major role. In this study, we investigated the inflammatory response of human neutrophils in an in vitro model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments. Methods: After separation of neutrophils from the whole blood, they were divided into 3 experimental groups: normoxianormoxia, hypoxia-normoxia, and hypoxia-hyperoxia groups. The production of H2O2, the expression of Toll-like receptor 4 (TLR4) receptor, and the extent of apoptosis of the neutrophils were checked. Results: The in vitro hypoxia-normoxia and-hyperoxia models, which simulated the PCAS, showed initiation of the neutrophils' inflammatory reaction by hypoxia insult. Lipopolysaccharide amplifies such inflammation; therefore, prevention of secondary infection may be critical in postresuscitation patients. Temporary hyperoxia following hypoxic insult showed no difference in inflammatory reaction compared with hypoxia-normoxia. Rather, temporary hyperoxia may suppress or minimize inflammation by attenuation of TLR4 receptor. Conclusion: It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100% O2 in a clinical situation may be helpful.

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