Interleukin-8 and Markers of Neutrophil Degranulation in Pleural Effusions

Abstract

In order to know the degree of interleukin-8 (IL-8) production in the pleural space and its relationship to neutrophil activation, IL-8, neutrophil elastase (NE), and myeloperoxidase (MPO) were assessed in blood and pleural fluid (PF) of 219 patients with pleural effusions. Correlations between blood and PF IL-8, NE, and MPO were either absent or weak, except for IL-8 in transudates (r = 0.6745, p < 0.001). PF IL-8, NE, and MPO concentrations in cases of empyema were higher than in cases of effusion of other causes (p < 0.001). No significant differences in inflammatory markers were observed between parapneumonic and tuberculous fluids. IL-8, NE, and MPO levels in malignant, nonspecific, and transudative effusions were lower than in those due to infection, the lowest levels corresponding to transudates. No significant correlation was observed between PF IL-8 and neutrophil count in any group; in contrast, IL-8 was associated with NE and MPO in empyema (r = 0.7545, and r = 0.7283; p < 0.001), tuberculosis (r = 0.4016, p = 0.008 and r = 0.6545, p < 0.001), and nonspecific effusions (r = 0.3748, p = 0.007 and r = 0.3085, p = 0.028). Our results indicate that local production of markers of the nonspecific inflammatory response is high in both chronic and acute pleural infection, and suggest a role for IL-8 in the release of NE and MPO.

Epithelial neutrophil-activating peptide-78 recruits neutrophils into pleural effusion

“…The effect of ENA-78 on neutrophil degranulation has been demonstrated in vitro [9,33] and there are also data to support its occurrence in vivo [25]. In agreement with earlier studies reported by other authors, we found the highest PE concentrations of both MPO and NE in infectious PEs [34], with a profile similar to that for ENA-78. In the present study, we have shown that both MPO and NE correlated positively with ENA-78, thus suggesting a role for ENA-78 in pleural neutrophil degranulation.…”

Pleural-fluid myeloperoxidase in complicated and noncomplicated parapneumonic pleural effusions

“…After excluding purulent effusions, pleural-fluid MPO was still the marker that best differentiated between the two types of PPE, with a sensitivity of 87.5% and a specificity of 85.1% at a cut-point limit of 3.000 mg?L -1 . The differences in mean levels of MPO between a previous report [13] and this study, are due to the inclusion of four additional cases in each subgroup of PPE. The aim of the previous report was to study whether interleukin (IL)-8 was produced in the pleural space and its relation to the neutrophil activation state in infected pleural fluid.…”

“…Increased concentrations of MPO have been reported in various inflammatory processes [10][11][12]. The authors previously detected higher levels of pleuralfluid MPO in complicated bacterial effusions than in noninfective effusions [13].…”

Metalloproteinases and tissue inhibitors of metalloproteinases in exudative pleural effusions

“…The inflammatory response initiated by the mesothelium provokes increased vascular patency and the release of inflammatory mediators, e.g. interleukin (IL)-8 and tumour necrosis factor alpha (TNF)-a [11][12][13], thereby favouring the formation of exudative pleural effusion, invasion of the pleural space by inflammatory cells and the release of neutrophil degranulation products, such as polymorphonuclear elastase (PMN-E) [14]. The fibrinolytic system is regulated by two plasminogen activators (PAs), tissue PA (t-PA) and urokinase PA (u-PA), and by plasminogen activator inhibitor type 1 (PAI-1) and 2 (PAI-2).…”