Downregulatory cytokines in tracheobronchial aspirate fluid from infants with chronic lung disease of prematurity

Abstract

We have demonstrated a sustained increase of TGF-beta1 levels in TAF from preterm infants who develop CLD, suggesting an important role for TGF-beta1 in the fibrotic response in the CLD lung. The elevated TGF-beta1 levels, combined with an absent or irregular secretion of IL-4, IL-10 and IL-12, can have importance for the increased tendency for the development of CLD in preterm infants.

TNF-a and IL-10 levels in tracheobronchial lavage of ventilated preterm infants and subsequent lung function

“…We did not detect a specific pattern of TNF-α or IL-10 production during the mechanical ventilation period, as has also shown in previous studies (4,9,22,(28)(29)(30).…”

“…Corso et al www.bjournal.com.br lower airway viral infections, with recurrent hospital admissions in early life (5,6). Premature rupture of membranes, inflammatory response to infections, mechanical ventilation, and supplemental oxygen have been implicated as causative perinatal events associated with persistent respiratory morbidity in this group of patients (7)(8)(9)(10)(11)(12)(13).…”

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

“…[1][2][3][4][5][6][7][8] Since inflammation is a fundamental pathologic feature of CLD, the genetic variants of cytokine genes may be good candidates to explain some of the individual variation in the development of this complication. TNF-a is a central mediator in the inflammatory cascade and TA concentrations are elevated in infants who develop CLD.…”

“…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.…”

Pulmonary inflammation and bronchopulmonary dysplasia

“…76 In preterm infants with BPD, increased levels of TGF-b have been detected in the airway secretions. [77][78][79] Using the data of the inhibitory effects of TGF-b levels on normal lung development, it can be speculated that interference of this cytokine with lung growth and suboptimal levels of different growth factors may also add to the pathogenesis of 'new BPD' and its possible long-term consequences. In fact, low airway concentrations of keratinocyte growth factor and hepatocyte growth factor were found to be associated with more severe lung disease in preterm infants.…”