The role of PMN apoptosis delay in acute lung injury induced by administrating LPS
Liu, R.; Xiao, N.; Tian, K.
Zhonghua Yi Xue Za Zhi 81(10): 617-621
2001
ISSN/ISBN: 0376-2491 PMID: 11798936 Document Number: 527393
To investigate the law of apoptosis and necrosis of the peripheral PMN and the PMN extravasated into pulmonary tissue, and its relationship with lung injury and the mechanisms involved. Fifty rats were subjected to acute lung injury by administrating intraperitoneally LPS (O(55)B(5), 3 mg/kg). Blood was harvested and bronchoalveoli was lavaged pre-LPS and 2, 4, 8, 12 h after LPS administration. PMNs were isolated by density gradient centrifugation and apoptosis, necrosis and respiratory burst were detected by flow cytometry. LDH activity, TNF, IL-1beta, IL-6, and lung permeability index were also measured. Viable PMN in bronchoalveolar lavage fluid (BLF) increased and apoptosis was delayed compared with that in peripheral blood. Meanwhile, TNF, IL-1beta and IL-6 in BLF were obviously higher and endured longer compared with those in peripheral blood. Moreover, the LDH activity in BLF and the lung permeability index were also remarkably increased. Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably caused by higher level cytokines and temporal increased of intracellular free Ca(2+) generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury.