PMN apoptosis and its relationship with the lung injury after chest impact trauma.
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.
Liu
Ren
R
Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China. liu0916@mail.china.com
Li
Shuang-ding
SD
Min
Jia-xin
JX
Xiao
Nan
N
Jiang
Qi-sheng
QS
Tian
Kun-lun
KL
Diao
You-fang
YF
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D055370:Lung Injury; D009504:Neutrophils / Q000502:physiology*; D011817:Rabbits; D016897:Respiratory Burst / Q000502:physiology; D013898:Thoracic Injuries / Q000150:complications*