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Increased NGF During Lung Ischemia and Reperfusion and Its Effect on MIP‐2 Production by Alveolar Macrophages

To assess its role as a potential inflammatory mediator, nerve growth factor (NGF) levels were measured during lung ischemia and reperfusion (I/R). Long Evans rats underwent 90 minutes of unilateral left lung ischemia and four hours of reperfusion. Sham animals underwent an identical surgical procedure without ischemia. During reperfusion, NGF levels significantly increased in the ischemic and nonischemic contralateral lung. Alveolar macrophages are activated by I/R and respond by producing chemokines and other inflammatory mediators; therefore, the ability of NGF to affect MIP‐2 production was examined in these cells as they express NGF receptors. Treatment of alveolar macrophage cell cultures with beta‐NGF in the presence of LPS increased MIP‐2 production. NGF significantly enhanced LPS‐induced MIP‐2 production after 4 hours (50%) and 24 hours (32%) although NGF alone had no effect on MIP‐2 production. Cell cultures pretreated with NGF prior to LPS stimulation produced more MIP‐2. To determine whether this increase in MIP‐2 production might be due to altered ERK phosphorylation, cells were serum‐starved for 1 hour and then treated with NGF in the absence and presence of LPS. After 30 minutes, maximal ERK phosphorylation was observed in cultures treated with both NGF and LPS in contrast to LPS alone where ERK phosphorylation peaked later at 60 minutes. These data suggest that increased NGF production during lung I/R may potentiate macrophage MIP‐2 production by enhancing ERK activation.