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Neutrophil Apoptosis in the Lung After Hemorrhage or Endotoxemia^*

Apoptosis and Migration Are Independent of Interleukin-1ß

^* From the University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Denver, CO.

Correspondence to: Merdad V. Parsey, MD, PhD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 E Ninth Ave, Denver, CO 80262

Hemorrhage and endotoxemia are associated with neutrophil accumulation in the lungs and the development of acute inflammatory lung injury. Because alterations in the rate of apoptosis may affect the number and function of neutrophils in the lungs, we determined the percentage of neutrophils undergoing apoptosis in the lungs of control, hemorrhaged, or endotoxemic mice. In control mice, 18.5 ± 1.2% of pulmonary neutrophils were apoptotic. The proportion of apoptotic neutrophils in the lungs was significantly decreased 1 h after hemorrhage (6.5 ± 1.6%, p < 0.01 compared with control) or endotoxemia (7.0 ± 0.9%, p < 0.01 compared with control). Between 1 and 24 h after endotoxemia or hemorrhage, the proportion of apoptotic neutrophils in the lung remained significantly depressed compared with that in control, unmanipulated mice. By 48 h, the proportion of apoptotic neutrophils returned to baseline levels in the lungs of hemorrhaged (21.4 ± 1.4%) or endotoxemic (16.4 ±1.6%) mice. Since increased production of interleukin-1ß (IL-1ß) appears to be important in the progression to acute inflammatory lung injury and can decrease the rate of neutrophil apoptosis, we examined IL-1ß expression in neutrophils isolated from the lungs of hemorrhaged and endotoxemic mice. Lung neutrophil IL-1ß messenger RNA was significantly increased from that of control mice (ie, 0.12 ± 0.06 relative absorbance units [RAU]) 1 h after hemorrhage (5.19 ± 0.068 RAU, p < 0.05 compared with control) or endotoxemia (8.90 ± 1.53 RAU, p < 0.01 compared with control). To determine the role of IL-1ß in the accumulation of neutrophils in the lung and on decreased apoptosis after hemorrhage or endotoxemia, we used mice genetically deficient in IL-1ß. In IL-1ß-deficient mice, there was no significant difference in lung neutrophil apoptosis or neutrophil entry into the lung after hemorrhage or endotoxemia compared with wild-type mice.

Our results show that apoptosis among lung neutrophils is decreased for the first 24 h after hemorrhage or endotoxemia. Although IL-1ß expression is increased in lung neutrophils under these conditions, IL-1ß is not responsible for either the influx of neutrophils into the lung or the reduction of apoptosis in neutrophil populations after hemorrhage or endotoxemia.

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