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Updated: Aug 19, 2026

Pseudofracture: An Acute Peripheral Tissue Trauma Model
Published on: April 18, 2011
Altered calcium regulation and function of human neutrophils during multiple trauma
S Rose1, M Illerhaus, A Wiercinski
1University of Saarland, Department of Trauma, Hand and Reconstructive Surgery, Homburg/Saar, Germany.
Abstract:
Altered intracellular Ca2+ concentration is a pivotal regulatory mechanism of leukocyte function. Since polymorphonuclear neutrophils (PMN) are involved in traumatic organ dysfunction, we prospectively investigated Ca2+ regulation and function of circulating PMN multiple trauma patients (Group A: ISS < 27; Group B: ISS > or = 27). Circulating PMN were isolated during 12 days, followed by determination of formyl-methionyl-leucyl-phenylalanine (fMLP)-induced PMN-superoxide production (PMN-SOP) by SOD-inhibitable ferricytochrome C reduction, and PMN cytosolic Ca2+ concentration ([Ca2+]i) by fluorescent fura2/AM (340/380 ratio). PMN-SOP was significantly higher in Group B (mean ISS: 39.9 +/- 2; n = 21) at day of admission than in controls and Group A (mean ISS: 18.2 +/- 1; n = 22) (P< 0.05). In Group B, the significant rise of basal [Ca2+]i between Day 2 and Day 4 was associated with significant lower PMN-SOP during that period (P < 0.05). The fMLP-induced [Ca2+]i response was supranormal in both groups. PMN-elastase concentrations were substantially higher in Group B compared with Group A until Day 4. Circulating IL-6, IL-8, and soluble TNF-receptor (55 kD) were significantly increased in Group B compared with Group A at the day of trauma (P < 0.05). Severe trauma is characterized by a biphasic pattern of neutrophil priming characterized by early increase and secondary suppression. The association of depressed neutrophil superoxide production (deactivation) and elevated basal [Ca2+]i suggests Ca2+-mediated disturbance of neutrophil NADPH-oxidase metabolism.
Insights
Severe trauma alters neutrophil function by affecting intracellular calcium (Ca2+) regulation. Elevated basal Ca2+ in neutrophils correlates with reduced superoxide production, suggesting Ca2+-mediated disturbances in NADPH-oxidase metabolism following trauma.
Area of Science:
- Immunology
- Cellular Biology
- Trauma Research
Background:
- Intracellular calcium (Ca2+) concentration is crucial for leukocyte function.
- Polymorphonuclear neutrophils (PMN) play a role in traumatic organ dysfunction.
Purpose of the Study:
- To investigate Ca2+ regulation and function of circulating PMN in multiple trauma patients.
- To compare PMN function and Ca2+ levels between trauma severity groups (ISS < 27 and ISS ≥ 27).
Main Methods:
- Prospective study of circulating PMN isolation over 12 days.
- Measurement of formyl-methionyl-leucyl-phenylalanine (fMLP)-induced PMN-superoxide production (PMN-SOP).
- Determination of PMN cytosolic Ca2+ concentration ([Ca2+]i) using fura2/AM.
Main Results:
- PMN-SOP was significantly higher in severe trauma patients (Group B) on admission.
- Elevated basal [Ca2+]i in Group B between Day 2 and Day 4 was associated with lower PMN-SOP.
- fMLP-induced [Ca2+]i response was supranormal in both groups; PMN-elastase, IL-6, IL-8, and soluble TNF-receptor were higher in Group B.
Conclusions:
- Severe trauma exhibits a biphasic pattern of neutrophil priming with early increase and secondary suppression.
- Elevated basal [Ca2+]i in neutrophils suggests Ca2+-mediated disturbance of NADPH-oxidase metabolism.
- These findings highlight Ca2+ dysregulation's role in neutrophil dysfunction post-severe trauma.
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