Neutrophil apoptosis in the acute respiratory distress syndrome

被引:306
作者
MatuteBello, G
Liles, WC
Radella, F
Steinberg, KP
Ruzinski, JT
Jonas, M
Chi, EY
Hudson, LD
Martin, TR
机构
[1] SEATTLE VA MED CTR, MED RES SERV, SEATTLE, WA 98108 USA
[2] UNIV WASHINGTON, HARBORVIEW MED CTR, PULM & CRIT CARE MED SECT, SEATTLE, WA 98104 USA
[3] UNIV WASHINGTON, SCH MED, DIV PULM & CRIT CARE MED, SEATTLE, WA USA
[4] UNIV WASHINGTON, SCH MED, DIV INFECT DIS, SEATTLE, WA USA
[5] UNIV WASHINGTON, SCH MED, DEPT MED, SEATTLE, WA 98195 USA
[6] UNIV WASHINGTON, SCH MED, DEPT PATHOL, SEATTLE, WA 98195 USA
关键词
D O I
10.1164/ajrccm.156.6.96-12081
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Little is known about neutrophil (PMN) apoptosis in the acute respiratory distress syndrome (ARDS). We used morphologic criteria to count apoptotic PMN in bronchoalveolar ravage fluid (BAL) of 35 patients on Days 1, 3, 7, 14, and 21 of ARDS and 13 patients on Days 1 and 3 of risk for ARDS. We found that the proportion of apoptotic PMN in BAL was low throughout the course of ARDS. There was no significant difference between the percentage of apoptotic PMN in patients at risk and patients with established ARDS or between patients who lived (2.4%) and patients who died (1.8%). When normal human PMN were incubated in ARDS BAL, a significantly lower proportion became apoptotic (50 +/- 4%), as compared with PMN incubated in lavage fluid from normal volunteers (76 +/- 7%, p < 0.05). This antiapoptotic effect of ARDS BAL was blocked by immunodepleting BAL of G-CSF and GM-CSF. We conclude that the proportion of apoptotic PMN recovered from the lungs of patients with ARDS is low throughout the course of ARDS. Furthermore, BAL from patients with ARDS prolongs survival of normal human PMN in vitro, and this effect is partially mediated by C-CSF and GM-CSF.
引用
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页码:1969 / 1977
页数:9
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