Interleukin-6, interleukin-8, and soluble tumor necrosis factor receptor-I in the cord blood as predictors of chronic lung disease in premature infants
“…Previous studies using oxygen dependence on d 28 to define BPD showed a significant association between cord blood cytokine levels and the development of BPD (22,23). Whereas cytokine levels were comparable between moderate/severe BPD and no/mild BPD in our series, we also found that cord blood IL-6 and IL-8 levels were significantly higher in BPD infants than those in no BPD infants.…”
contrasting
confidence: 38%
“…Several subsequent studies have investigated various inflammatory cytokines in both cord blood and bronchoalveolar lavage fluid just after birth in infants who subsequently developed BPD (21), and some of these studies have demonstrated that cord blood levels of IL-6 and other cytokines may be useful for predicting the development of BPD (22,23). Therefore, to compare KL-6 with other markers, we also measured IgM and various cytokines [including IL-1, IL-6, TNF-␣, IL-8, and macrophage inflammatory protein (MIP)-1␣] in the cord blood.…”
Circulating KL-6 is a specific indicator of pulmonary injury affecting the alveolar epithelium and interstitium. Our preliminary study suggested the usefulness of plasma KL-6 as a marker of bronchopulmonary dysplasia (BPD). To confirm the diagnostic value of KL-6 for BPD as well as to determine the reference range, we conducted a larger prospective study in 135 preterm infants Ͻ32 wk GA. Among the infants without oxygen dependence at a postconceptional age of 36 wk, the plasma KL-6 level showed no significant association with GA at any time. Among 42 infants Ͻ28 wk GA, plasma KL-6 levels were significantly higher in those with moderate/ severe BPD compared with those with no/mild BPD. A plasma level of 199 U/mL at 1 wk or 232 U/mL at 2 wk was an excellent predictor of moderate/severe BPD Ͻ28 wk GA (positive predictive value of 83% and 80%, respectively). Unlike nonspecific markers of inflammation or fibrosis, KL-6 objectively reflects the severity of pulmonary injury irrespective of the treatment or the radiographic changes. Therefore, not only as a good marker, measurement of KL-6 may also help to provide new insights into the pathogenesis of BPD.
“…Previous studies using oxygen dependence on d 28 to define BPD showed a significant association between cord blood cytokine levels and the development of BPD (22,23). Whereas cytokine levels were comparable between moderate/severe BPD and no/mild BPD in our series, we also found that cord blood IL-6 and IL-8 levels were significantly higher in BPD infants than those in no BPD infants.…”
contrasting
confidence: 38%
“…Several subsequent studies have investigated various inflammatory cytokines in both cord blood and bronchoalveolar lavage fluid just after birth in infants who subsequently developed BPD (21), and some of these studies have demonstrated that cord blood levels of IL-6 and other cytokines may be useful for predicting the development of BPD (22,23). Therefore, to compare KL-6 with other markers, we also measured IgM and various cytokines [including IL-1, IL-6, TNF-␣, IL-8, and macrophage inflammatory protein (MIP)-1␣] in the cord blood.…”
Circulating KL-6 is a specific indicator of pulmonary injury affecting the alveolar epithelium and interstitium. Our preliminary study suggested the usefulness of plasma KL-6 as a marker of bronchopulmonary dysplasia (BPD). To confirm the diagnostic value of KL-6 for BPD as well as to determine the reference range, we conducted a larger prospective study in 135 preterm infants Ͻ32 wk GA. Among the infants without oxygen dependence at a postconceptional age of 36 wk, the plasma KL-6 level showed no significant association with GA at any time. Among 42 infants Ͻ28 wk GA, plasma KL-6 levels were significantly higher in those with moderate/ severe BPD compared with those with no/mild BPD. A plasma level of 199 U/mL at 1 wk or 232 U/mL at 2 wk was an excellent predictor of moderate/severe BPD Ͻ28 wk GA (positive predictive value of 83% and 80%, respectively). Unlike nonspecific markers of inflammation or fibrosis, KL-6 objectively reflects the severity of pulmonary injury irrespective of the treatment or the radiographic changes. Therefore, not only as a good marker, measurement of KL-6 may also help to provide new insights into the pathogenesis of BPD.
“…To elucidate the role of cytokines, especially IL -8 and IL -6, in the development of chronic lung disease (CLD) of the neonates, serial and simultaneous measurement of cytokines in the serum and the tracheobronchial aspirate of low birth weight infants were conducted 10) . The cord blood IL -6 and IL -8 levels of CLD of the neonates with fetal inflammatory response syndrome (FIRS) were significantly elevated, but those of CLD neonates without FIRS were not significantly different compared with non -CLD neonates with respiratory distress syndrome 11) . The IL -8 level of the tracheobronchial aspirate in neonates with CLD was higher than that of neonates without CLD on day 10 of age 10) .…”
A newborn male with pulmonary edema was delivered at term by elective Caesarian section. Cytokine profiles of 17 cytokines and KL -6 in cord blood and serial serum values were investigated. The cord blood values of all 17 cytokines and KL -6 were within normal limits. Subsequently, IL -6, IL -8, IL -10, IL -13, IL -17, and IFNγ rapidly elevated during the first several hours after birth and dramatically decreased thereafter, whereas KL -6 rose to 611 U/ml on the 3 rd day of life and then gradually decreased. These cytokines may induce pulmonary permeability, and KL -6 secreted in lining fluid could result in influx into the bloodstream. This is the first report that we have differentiated neonatal pulmonary edema from TTN by the measurement of serial cytokine profiles and KL -6 in serum.
“…Moreover, in those infants, a large number of activated neutrophils are found in the air spaces within hours after birth [Arnoon, S. et al (1993)]. The contribution of airway inflammation to the development of CLD of prematurity has been extensively studied [Jonsson, B. et al (1997), An, H. et al (2004), Bancalari, E. (2000), Groneck, P. & Speer, CP. (1995), McColm, JR. & McIntosh, N. (1994)].…”
Section: Oxidative Stress and Lung Injurymentioning
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