Increase in interleukin-8 and soluble intercellular adhesion molecule-1 in bronchoalveolar lavage fluid from premature infants who develop chronic lung disease.

Abstract

Interleukin-8 (IL-8), soluble intercellular adhesion molecule-i (sICAM), elastase and neutrophils were assessed in bronchoalveolar lavage fluid from nine infants who developed chronic lung disease (CLD) after respiratory distress syndrome (RDS), seven who had recovered from RDS, and in four control infants. IL-8, sICAM, elastase and neutrophils in bronchoalveolar lavage fluid were increased in the CLD group, the differences being most pronounced at 10 days of age. When babies with and without CLD were compared at 10 days of age, bronchoalveolar lavage fluid from the babies with CLD had significantly increased (114.0 vs 12*7 nglml), sICAM (19.0 vs 1*1 ,ug/ml), elastase (6.9 vs 0*9 ,ug/ml) and neutrophils (1.9 vs 0.4X109/1). In serum the increased concentration of IL-8 observed at birth in the CLD (247 pg/ml) and RDS (192 pg/ml) groups decreased over three weeks to the concentrations observed in the controls (<70 pg/ml). Persistent inflammation could be a major contributory factor in the development of CLD.

Angiopoietin 2 concentrations in infants developing bronchopulmonary dysplasia: attenuation by dexamethasone

“…Infants who developed BPD had significantly increased concentrations of soluble intracellular adhesion molecule-1, [19][20][21] tumor necrosis factor-a, 22 interleukin (IL)-1b, 22 28,29 transforming growth factor-b-1, 30 fibroblast growth factor-2 31 and endothelin-1. 24 Others have been unable to confirm IL-1b, IL-6, macrophage inflammatory protein-1-a, -b and endothelin-1 31 in the TA as markers for BPD.…”

“…These include soluble intracellular adhesion molecule-1, IL-1b, IL-6 and IL-8. 17,19,20,[22][23][24][25][26]28 In contrast, conflicting results have been reported for VEGF 31,36 and endothelin-1 24,31 TA values in VPIs at risk of developing BPD. Thus, it is difficult to discern the clinical utility of such measurements of a majority of cytokines unless it has been consistently replicated in disparate populations, using standard definitions and techniques.…”

Pulmonary inflammation and bronchopulmonary dysplasia

“…Preterm infants with various stages of developing BPD had much higher and persisting numbers of inflammatory cellsneutrophils and macrophages -in their bronchoalveolar lavage fluid (BALF) compared with infants who recovered from RDS. [6][7][8][9][10] A neutrophil influx into the airways was observed immediately after initiation of ventilation and was associated with a decrease in the number of circulating neutrophils. This phenomenon was shown to correlate with the extent of pulmonary edema formation and an increased risk of developing BPD.…”

The TNF−α –308, MCP−1 –2518 and TGF−β1 +915 polymorphisms are not associated with the development of chronic lung disease in very low birth weight infants

“…Increased concentrations of inflammatory mediators in airway secretions during the first week of life have been associated with the development of CLD in the preterm infant suggesting that inflammation plays a central role in this condition. [1][2][3][4][5][6][7][8] Concentrations of tumor necrosis factor-a (TNF-a), a central mediator in the inflammatory cascade, are elevated during the first week of life in the tracheal aspirates (TA) obtained from infants who subsequently develop CLD. 1,2 The magnitude of TNF-a production may be in part genetically determined.…”