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Published on: October 29, 2014
PMN apoptosis and its relationship with the lung injury after chest impact trauma
Ren Liu1, Shuang-ding Li, Jia-xin Min
1Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China. liu0916@mail.china.com
Background:
Polymorphonuclear neutrophil (PMN), one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma.
Methods:
PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, lactate dehydrogenase and (LDH) [Ca2+]i were measured.
Results:
The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma, and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile, lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control (P < 0.05) from 4 hours to 24 hours, and intracellular free Ca2+ in PMN was increased temporarily.
Conclusions:
Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporary increase of intracellular free Ca2+ may be responsible for the delayed apoptosis of PMN.
Insights
Delayed polymorphonuclear neutrophil (PMN) apoptosis after chest trauma contributes to lung injury. This PMN dysfunction, potentially driven by increased intracellular calcium, exacerbates inflammation and tissue damage.
Area of Science:
- Immunology
- Trauma Research
- Cell Biology
Background:
- Polymorphonuclear neutrophils (PMNs) are key inflammatory cells involved in all phases of inflammation.
- Chest impact trauma can lead to significant inflammatory responses and tissue damage.
Purpose of the Study:
- To investigate the relationship between PMN apoptosis and lung injury following chest impact trauma.
- To understand the role of PMN behavior in the inflammatory process post-trauma.
Main Methods:
- PMNs were isolated from rabbits experiencing chest impact trauma.
- Apoptosis, necrosis, survival, and respiratory burst of PMNs were analyzed using flow cytometry.
- Lactate dehydrogenase (LDH) levels and intracellular calcium ([Ca2+]i) were measured.
Main Results:
- Delayed PMN apoptosis and increased viable cells were observed between 2 and 12 hours post-trauma.
- PMN respiratory burst activity significantly increased from 2 hours, peaking at 8 hours.
- Elevated LDH and transient increases in intracellular free Ca2+ in PMNs were noted post-trauma.
Conclusions:
- Impaired PMN apoptosis and retention in tissues lead to sustained PMN activation and release of damaging substances.
- The observed increase in intracellular free Ca2+ may be a key factor in the delayed PMN apoptosis.
- These findings highlight PMN apoptosis as a critical determinant of lung injury severity after chest trauma.
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