Increase in the concentration of transforming growth factor beta-1 in bronchoalveolar lavage fluid before development of chronic lung disease of prematurity

Kotecha, Sailesh; Wangoo, A.; Silverman, Michael; Shaw, Rory

doi:10.1016/s0022-3476(96)70355-4

Cited by 180 publications

(122 citation statements)

References 20 publications

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“…While one study has shown that TA specimens may be the suitable substitute for bronchoalveolar lavage samples in preterm infants, 37 there has been some controversy regarding whether the measurements of these markers in the TA need to be 'normalized' for them to be valid. While some have advocated the use of total protein, 12,38 secretory component of immunoglobulin A 29,39 -43 and serum urea 17,30 for the same, others have espoused that no 'normalization' is required. 31,44 -46 This study has reported Ang2 values normalized to total protein to correct for dilution.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2007

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Objectives: To study the association between angiopoietin 2 (Ang2) concentrations in tracheal aspirates (TAs) and adverse outcome (bronchopulmonary dysplasia (BPD)/death) in ventilated premature infants (VPIs) and modulation of Ang2 concentrations with dexamethasone (Dex) use.Study Design: Serial TA samples were collected on days 1, 3, 5 and 7, and Ang2 concentrations were measured. Ang2 TA concentrations were compared prior to and after 48 to 72 h of using Dex.Result: A total of 151 TA samples were collected from 60 VPIs. BPD was defined as the oxygen requirement at 36 weeks postmenstrual age (PMA). Twelve infants (mean ± s.d.) (gestational age (GA) 26.5 ± 2.1 weeks, birth weight (BW) 913±230 g) had no BPD, 32 infants (GA 25.8±1.4 weeks, BW 768 ± 157 g) developed BPD and 16 infants (GA 24.5 ± 1.1 weeks, BW 710 ± 143 g) died before 36 weeks PMA. Ang2 concentrations were significantly lower in infants with no BPD (median, 25th and 75th percentile) (157, 16 and 218 pg mg À1 ) compared with those who developed BPD (234, 138 and 338 pg mg À1 , P ¼ 0.03) or BPD and/or death (234, 157 and 347 pg mg À1 , P ¼ 0.017), in the first week of life. Twenty-six VPIs (BW 719±136 g, GA 25.1±1.3 weeks) received 27 courses of Dex. Ang2 concentrations before starting Dex were 202, 137 and 278 pg mg À1 and significantly decreased to 144, 0 and 224 pg mg À1 after therapy (P ¼ 0.007).Conclusions: Higher Ang2 concentrations in TAs are associated with the development of BPD or death in VPIs. Dex use suppressed Ang2 concentrations.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2007

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“…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.…”

Section: Inflammatory Cells Endothelial Interactions and Chemotaxismentioning

confidence: 99%

Pulmonary inflammation and bronchopulmonary dysplasia

Speer

2006

J Perinatol

130

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Various pre-and postnatal risk factors, which act additively or synergistically induce an injurious inflammatory response in the airways and the pulmonary interstitium of preterm infants with bronchopulmonary dysplasia. This inflammatory response is characterized by an accumulation of neutrophils and macrophages as well as an arsenal of proinflammatory mediators that affect the endothelium and alveolar-capillary integrity. Besides proinflammatory cytokines and toxic oxygen radicals, lipid mediators as well as potent proteases may be responsible for acute lung injury. There is increasing evidence that an imbalance between pro-and anti-inflammatory factors, which should protect the alveoli and lung tissue, are key features in the pathogenesis of bronchopulmonary dysplasia. In addition, a subnormal generation of growth factors may affect alveolarization and vascular development in preterm infants with bronchopulmonary dysplasia. In this condensed review article, the current concepts on the possible role of inflammation in the evolution of bronchopulmonary dysplasia will be summarized.

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“…Lung morphology is markedly perturbed in infants with BPD, often characterized by failure to form alveoli and disruption of the peripheral pulmonary blood vessels (Husain et al, 1998). Increased concentrations of TGF-␤ were observed in lung lavage fluid and lung tissue from infants with BPD, suggesting a potential role of TGF-␤ in the pathogenesis of this disorder (Kotecha et al, 1996;Lecart et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

Zeng

Gray

Stahlman

et al. 2001

Developmental Dynamics

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Members of the transforming growth factor ␤ (TGF-␤) family of polypeptides have been implicated in morphogenesis and differentiation in numerous tissues, including the lung. In order to further define effects of TGF-␤ signaling in lung morphogenesis, a constitutively active form of TGF-␤1 was expressed in respiratory epithelial cells of the fetal mouse lung in vivo. Expression of TGF-␤1 arrested lung morphogenesis in the pseudoglandular stage of development, inhibiting synthesis of differentiation-dependent proteins, SP-B, SP-C, and CCSP, and maintaining embryonic patterns of staining for thyroid transcription factor-1 (TTF-1) and hepatocyte nuclear factor-3␤ (HNF-3␤). The pulmonary mesenchyme was thickened and vascular density was increased by TGF-␤1. TGF-␤1 decreased expression of vascular endothelial growth factor-A (VEGF-A) mRNA and protein, and the abundance of Flk-1 mRNA in the lung mesenchyme. Distribution of platelet-endothelial cell adhesion molecule (PECAM)-1, a marker of pulmonary blood vessels, was altered, and ultrastructural studies demonstrated that TGF-␤1 inhibited vascular development in the fetal lung. TGF-␤1 perturbed both epithelial cell differentiation and formation of the pulmonary vasculature, supporting the concept that precise control of signaling via the TGF-␤ receptor pathway is critical for normal lung morphogenesis.

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Increase in the concentration of transforming growth factor beta-1 in bronchoalveolar lavage fluid before development of chronic lung disease of prematurity

Cited by 180 publications

References 20 publications

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

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

Pulmonary inflammation and bronchopulmonary dysplasia

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

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