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.

[The inflammatory mediators induced endothelial cell injury through delay neutrophils apoptosis].

This study aimed at elucidating the relationship between NTP apoptosis and endothelial cell injury. After isolation and purification, activated NTPs were incubated with endothelial cells directly or indirectly contact in a ratio of 5:1 and 10:1, meanwhile 10ng/ml IL-6 and 10% (v/v) burned serum added or not. Apoptosis and necrosis of endothelial cells were detected in situ. Activated NTP alone exerted no obviously detrimental effects on endothelial cells. However, when IL-6-or serum from burn patients was added, NTP apoptosis was delayed and endothelial cells were injured in the form of necrosis. Inflammatory mediators can delay NTP apoptosis, further research demonstrated that direct contact between the two types of cells was essential for NTP to impact injury on endothelial cells.