[The role of granulocyte colony-stimulating factor in pathogenesis of acute lung injury].
OBJECTIVE
To investigate the role of granulocyte colony-stimulating factor (G-CSF) in pathogenetic mechanism of acute lung injury (ALI) by endotoxin.


METHODS
A rat model of ALI was established by intraperitoneal injection of Escherichia coli LPS with a dose of 2 mg/kg. Thirty SD rats were randomly divided into the normal group and four endotoxin treated groups at different time intervals (2 h, 4 h, 6 h, 8 h after LPS injection), 6 rats each group. RT-PCR method was used to determine the expression level of G-CSF mRNA in lung tissue. The concentrations of serum TNF-alpha were determined by RIA. The number of neutrophils fixed in lung and peripheral blood neutrophils were counted, and pathological changes of lung tissue were examinted.


RESULTS
The level of G-CSF mRNA expression in lung tissue increased rapidly at 2 h after LPS injection, peaked at 4 h. Although decreased a little at 6 h and 8 h, it was still significantly different from the normal group and the 2 h group (P < 0.01, P < 0.05). The level of TNF-alpha peaked at 2 h after endotoxin injection, which was significantly different from the normal group (P < 0.05). The number of neutrophils fixed in the lung also increased in endotoxin-treated groups, and the level of G-CSF mRNA expression in the lung tissue was positively correlated with the number of neutrophils fixed in the lung, the lung coefficient and the pathological signs of lung injury.


CONCLUSIONS
The increase in the level of G-CSF mRNA expression in the lung tissue after endotoxin injection resulted in neutrophil sequestration in the lung, which may aggravate lung injury and increase lung coefficient. This process may be an important link in the pathogenetic mechanism of ALI induced by endotoxin.
Zhang
D
D
Respiratory Department on the South Building of P.L.A General Hospital, Beijing 100853, China.
Zhang
J
J
Liu
Y
Y
D000818:Animals; D004195:Disease Models, Animal; D016179:Granulocyte Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D008070:Lipopolysaccharides; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000097:blood* / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D012129:Respiratory Function Tests; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor