Airway and blood vessel interaction during lung development

Hislop, Alison A.

doi:10.1046/j.1469-7580.2002.00097.x

Cited by 243 publications

(210 citation statements)

References 61 publications

(94 reference statements)

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“…The respiratory system is permeated by a dual blood supply; the pulmonary circulation and the bronchial circulation [15]. The two circulatory systems are quite different physiologically and pharmacologically, including muscularisation at different levels and different arterial pressures: bronchial arterial (mean arterial) pressure and pulmonary artery pressure (~20 mmHg) [14,16].…”

Section: The Pulmonary Vasculature System Cellular Composition and Amentioning

confidence: 99%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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In chronic lung disorders such as in asthma and chronic obstructive pulmonary disease (COPD) there is increased bronchial angiogenesis and remodelling of pulmonary vessels culminating to altered bronchial and pulmonary circulation. The involvement of residential cells such as endothelial cells, smooth muscle cells and pulmonary fibroblasts, all appear to have a crucial role in the progression of vascular inflammation and remodelling. The regulatory abnormalities, growth factors and mediators implicated in the pulmonary vascular changes of asthma and COPD subjects and potential therapeutic targets have been described in this review.

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Section: The Pulmonary Vasculature System Cellular Composition and Amentioning

confidence: 99%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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“…Distal lung development in these extremely premature infants, therefore, must continue after birth (Hislop, 2002). Postnatal development of the lung in premature infants frequently occurs abnormally, leading to bronchopulmonary dysplasia, a disease characterized by hypoxia, carbon dioxide retention, and altered pulmonary mechanics (Bancalari et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Toll‐like receptor signaling inhibits structural development of the distal fetal mouse lung

Prince

Dieperink

Okoh

et al. 2005

Developmental Dynamics

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We tested the hypothesis that innate immune signaling in utero could disrupt the structural development of the fetal lung, contributing to the pathogenesis of bronchopulmonary dysplasia. Injection of Escherichia coli lipopolysaccharide (LPS) into the amniotic fluid of E15 BALB/cJ mice increased the luminal volume density of fetal mouse lungs at embryonic day (E) 17 and E18. LPS also increased luminal volume and decreased distal lung branching in fetal mouse lung explants. This effect required NF-B activation and functional Toll-Like Receptor 4. Airway branching may require fibronectin-dependent epithelial-mesenchymal interactions, representing a potential target for innate immune signaling. Anti-fibronectin antibodies and LPS both blocked distal lung branching. By immunofluorescence, fibronectin localized to the clefts between newly formed airways but was restricted to peripheral mesenchymal cells in LPS-exposed explants. These data suggest that LPS may alter the expression pattern of mesenchymal fibronectin, potentially disrupting epithelial-mesenchymal interactions and inhibiting distal airway branching and alveolarization. This mechanism may link innate immune signaling with defects in structural development of the fetal lung. Developmental Dynamics 233:553-561, 2005.

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“…Animal studies have not assessed preterm survivors beyond a human equivalent of 3 years of age (9). Because human alveolarization was thought to be complete by 3 years of age (13,14), the histologic data were extrapolated to postulate persistence of acinar damage in preterm and CLD survivors (9, 15).…”

mentioning

confidence: 99%

Catch-up Alveolarization in Ex-Preterm Children. Evidence from ³He Magnetic Resonance

Narayanan

Beardsmore

Owers‐Bradley

et al. 2013

Am J Respir Crit Care Med

130

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Rationale: Histologic data from fatal cases suggest that extreme prematurity results in persisting alveolar damage. However, there is new evidence that human alveolarization might continue throughout childhood and could contribute to alveolar repair. Objectives: To examine whether alveolar damage in extreme-preterm survivors persists into late childhood, we compared alveolar dimensions between schoolchildren born term and preterm, using hyperpolarized helium-3 magnetic resonance. Methods: We recruited schoolchildren aged 10-14 years stratified by gestational age at birth (weeks) to four groups: (1) term-born (37-42 wk; n ¼ 61); (2) mild preterm (32-36 wk; n ¼ 21); (3) extreme preterm (,32 wk, not oxygen dependent at 4 wk; n ¼ 19); and (4) extreme preterm with chronic lung disease (,32 wk and oxygen dependent beyond 4 wk; n ¼ 18). We measured lung function using spirometry and plethysmography. Apparent diffusion coefficient, a surrogate for average alveolar dimensions, was measured by helium-3 magnetic resonance. Measurements and Main Results: The two extreme preterm groups had a lower FEV 1 (P ¼ 0.017) compared with term-born and mild preterm children. Apparent diffusion coefficient was 0.092 cm 2 /second (95% confidence interval, 0.089-0.095) in the term group. Corresponding values were 0.096 (0.091-0.101), 0.090 (0085-0.095), and 0.089 (0.083-0.094) in the mild preterm and two extreme preterm groups, respectively, implying comparable alveolar dimensions across all groups. Results did not change after controlling for anthropometric variables and potential confounders. Conclusions: Alveolar size at school age was similar in survivors of extreme prematurity and term-born children. Because extreme preterm birth is associated with deranged alveolar structure in infancy, the most likely explanation for our finding is catch-up alveolarization.Keywords: alveolar structure; lung acinus; bronchopulmonary dysplasia; neonatal chronic lung disease Advances in preterm care have led to increased survival of extremely premature babies, with increasing numbers reaching adulthood. This has shifted the focus of research from survival toward long-term sequelae of prematurity (1, 2). Infants born extremely preterm are known to have arrested alveolar development, manifesting as fewer and larger alveoli (3, 4). Schoolage and adult survivors of extreme preterm birth are known to have long-term respiratory problems, particularly decreased forced expiratory volumes and increased residual lung volumes, suggesting airway damage (5, 6). There are insufficient data regarding structure and development of the periphery of the lung in long-term survivors of preterm birth because studies on this cohort have relied on traditional lung function tests that only provide an overall estimate of function.The short-and long-term outcomes described previously correlate with gestational age (GA) at birth and the presence of chronic lung disease of prematurity (CLD), one of the early pulmonary sequelae of extreme preterm birth (6-8). Most evidence regard...

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Airway and blood vessel interaction during lung development

Cited by 243 publications

References 61 publications

Pulmonary vascular changes in asthma and COPD

Pulmonary vascular changes in asthma and COPD

Toll‐like receptor signaling inhibits structural development of the distal fetal mouse lung

Catch-up Alveolarization in Ex-Preterm Children. Evidence from ³He Magnetic Resonance

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Airway and blood vessel interaction during lung development

Cited by 243 publications

References 61 publications

Pulmonary vascular changes in asthma and COPD

Pulmonary vascular changes in asthma and COPD

Toll‐like receptor signaling inhibits structural development of the distal fetal mouse lung

Catch-up Alveolarization in Ex-Preterm Children. Evidence from 3He Magnetic Resonance

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Catch-up Alveolarization in Ex-Preterm Children. Evidence from ³He Magnetic Resonance