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Lung Growth: Implications for the Newborn Infant Arch Dis Child Fetal Neonatal Ed: first published as 10.1136/fn.82.1.F69 on 1 January 2000. Downloaded from Arch Dis Child Fetal Neonatal Ed 2000;82:F69–F74 F69 CURRENT TOPIC Lung growth: implications for the newborn infant Sailesh Kotecha Introduction Table 1 Lung growth stages Modern neonatal practice has improved the outcome of extremely preterm infants. How- Time (weeks) ever, why some infants require prolonged peri- Embryonic 3–7 ods of respiratory support while others improve Canalicular 7–16 Pseudoglandular 16–26 after a short period of mechanical ventilation, Saccular 26–36 remains largely speculative. Many risk factors, Alveolar 36 weeks–2 years including barotrauma or volutrauma due to Postnatal growth 2–18 years mechanical ventilation, oxygen toxicity, and infection, have been identified for the develop- vessels continues, and by the end of this stage ment of chronic lung disease of prematurity the conducting airways, terminal bronchioles, (CLD). Attempts to minimise these with mod- and primitive acinus, are completed. The ern neonatal practice, including newer ventila- pseudo-stratified columnar epithelium is pro- tory techniques, have had minimal impact on gressively replaced by tall columnar cells in the its incidence. Factors other than barotrauma proximal airways and cuboidal cells in the dis- and oxygen toxicity are likely to be important tal acinar structures. in the development of CLD. During the canalicular stage, which occurs Although our understanding of normal fetal between 16 and 26 weeks in utero, further lung development has increased substantially development of the distal airways into defini- over the past few years, it nevertheless remains tive primary acini occurs. The acinar structures rudimentary, especially in infants who have consist of respiratory bronchioles, alveolar survived neonatal intensive care. Animal mod- ducts, and rudimentary alveoli. Development els have provided many clues to the eVects of of the intracinar capillaries, which are derived interventions in the neonatal unit on the lung from the surrounding mesenchyme, accompa- growth of preterm infants. Normal lung growth nies the evolution of the acinus. Lamellar bod- and some of the abnormalities that may result ies containing surfactant proteins and phos- from disordered growth or from medical inter- pholipid in type II pneumocytes can be ventions are reviewed in this article. There are observed lining the acinar tubules at this stage. a vast number of other factors which influence http://fn.bmj.com/ DiVerentiation into type I pneumocytes occurs lung growth—some, such as fetal breathing and in conjunction with the formation of the lung fluid dynamics, deserve reviews of their alveolar–capillary barrier. own. The saccular phase begins with marked enlargement of the peripheral airways as the Normal lung growth acinar tubules dilate and the walls thin, result- Normal lung development, which occurs as a ing in increased gas exchanging surface area. series of complex tightly regulated events, can Lamellar bodies in type II cells increase and on September 24, 2021 by guest. Protected copyright. be divided into a number of stages (table 1).1–3 further maturation into type I cells occurs. During the earliest embryonic stage, the lung Capillaries are closely associated with type I develops as an outgrowth of the ventral wall of cells, thus reducing the distance between the the primitive foregut endoderm. Epithelial cells future air–blood interface. from the foregut endoderm invade the sur- The secondary alveolar septa are formed rounding mesoderm to form the proximal during the alveolar stage, which occurs from 36 structures of the respiratory tract. Following weeks of gestation until at least 24 months the formation of the trachea and the main postnatally.5 The secondary septa consist of bronchi, the five lobes are formed, and by the projections of connective tissue and a double end of this stage, the 18 major lobules are rec- capillary loop. Alveolar formation and matura- ognisable. Current evidence suggests that the tion occur, with thinning of the alveolar walls surrounding mesoderm regulates the branch- and remodelling of the double capillary loops ing of the tracheobronchial tree.4 At the end of by apoptosis to form a single capillary loop.6 this stage, the pulmonary arteries develop from During this stage marked proliferation of all Department of Child the sixth aortic arches and accompany the cell types occurs. Mesenchymal cells proliferate Health, University of Leicester, branching airways. and deposit the necessary extracellular matrix. Leicester LE2 7LX The embryonic phase is followed by the Epithelial cells, especially type I and II S Kotecha pseudo-glandular stage—so-called because the pneumocytes, increase in numbers to line the Correspondence to: epithelial tubules are surrounded by thick mes- alveolar walls, and endothelial cells undergo Dr Sailesh Kotecha enchymal tissue. Branching of the airways and massive growth in the secondary septa with Arch Dis Child Fetal Neonatal Ed: first published as 10.1136/fn.82.1.F69 on 1 January 2000. Downloaded from F70 Kotecha subsequent remodelling to form a single capil- epithelial cell proliferation and the resulting lary loop from a double one. The net result is a branching of the airways. Disruption of its great increase in gas exchanging surface area receptor FGF-R2 in epithelial cells of the and maturation of cells which will respond to airways results in blockage of dichotomous the postnatal environment. branching of the conducting airways. By Due to the diYculties of estimating alveolar contrast, transforming growth factor â numbers at birth, numbers ranging from 20 (TGF-â) inhibits branching morphogenesis, million to 50 million have been quoted. A final epithelial cell growth, and diVerentiation of number of around 300 million is reached by fetal lung explants.11 TGF-â decreases with adulthood. increasing gestation, which removes the inhibi- tory eVects of this growth factor and allows Regulation of lung growth branching to proceed. Other growth factors Most of our knowledge about lung growth is which may be important are listed in table 2. A derived from the study of animals who often more comprehensive review of growth factors have very diVerent timing of morphological and their importance in normal lung growth is 4–7 lung growth compared with humans. For discussed elsewhere. instance, in sheep most of the alveolar develop- Many of these growth factors are produced ment occurs before birth. Rats and mice may by the mesenchyme surrounding the lung epi- be more useful models of human lung growth thelial cells. Indeed, the mesenchyme directs as most alveolar development occurs postna- the ultimate destiny of the epithelial cells. For tally. instance, salivary epithelium grown on mam- Despite widespread interest in this area, our mary mesenchyme results in mammary gland understanding of the mechanisms involved in morphology, and transposition of the bronchial normal lung growth remains limited.7 Table 2 mesenchymal to the peripheral airways results shows the increasing list of transcriptional and in a bronchial-like morphology. Further weight growth factors which are implicated in normal to the importance of the mesenchyme in lung growth. Hepatic nuclear factor- â directing the epithelial development is given by 3 the presence of the mRNA of growth factors in (HNF3â) seems to be required for the forma- tion of the foregut from which the primitive the mesenchyme and the corresponding pro- lung bud is derived.8 Genetic disruption of tein in epithelial cells—for example, KGF and IGF. The mesenchymal–epithelium interac- HNF3â disrupts formation of the foregut endoderm and its derivatives, including the tions may result from direct cell to cell contact lung.9 In human neonatal lung, it is present in by soluble molecules, including growth factors type II pneumocytes as well as ciliated and (paracrine) or by cell–extracellular matrix 10 interactions. non-ciliated epithelial cells. HNF3â also influences expression of other nuclear factors including thyroid transcription factor 1 (TTF- 1). TTF-1 mRNA is detected in rat primordial Factors which may aVect lung growth lung and the protein has been detected as early DEVELOPMENTAL ABNORMALITIES as 11 weeks of gestation in human lungs. Lung growth may be aVected by several factors. TTF-1 seems to increase expression of the sur- During development of the pulmonary tree, factant proteins, at least in vitro, and its laryngeal, tracheal, or oesophageal atresia; tra- ablation by genetic targeting impairs lung mor- cheal stenosis; tracheo-oesophageal atresia or http://fn.bmj.com/ phogenesis, resulting in hypoplastic lung with fistula; pulmonary agenesis; arterio-venous mal- poorly diVerentiated epithelium and poor gas formations or congenital lung cysts (including exchanging areas.7 Interactions between the bronchogenic cysts) may develop during the transcription factors are likely to be more com- embryonic stage. Pulmonary sequestration, pul- plex than described above and very tightly monary hypoplasia or lymphangectasia, con- regulated. genital cystic adenomatous malformations, and As with transcription factors, our under- lung cysts may develop during the pseudo- on September 24, 2021 by guest. Protected copyright. standing of the role of growth factors remains glandular stage. Failure of the pleuro-peritoneal in its infancy. The number of growth factors membranes to close at this stage may lead to the identified continues to increase (table 2), but
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