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PubMed2002

Expression profiling of the developing mouse lung: insights into the establishment of the extracellular matrix.

We have undertaken a comprehensive gene expression profiling of the entire process of murine lung development using oligonucleotide-based microarrays. Our data reveals the expression pattern of approximately 11,000 genes throughout the morphologic stages of lung development. This includes known genes with unappreciated pulmonary expression and novel genes with undefined functions. Traditional gene expression analysis techniques verify a high degree of confidence in the microarray data. Examination of the data confirms previously known patterns of expression for extracellular matrix genes and provides new information regarding relationships in temporal expression among groups of these genes. Large-scale cluster analysis reveals associations in the expression profile of specific genes with defined developmental processes. For instance, we identify groups of genes, which are coordinately expressed with extracellular matrix genes during lung development. These data should serve as a resource for the pulmonary research community and assist in deciphering the molecular mechanisms governing normal lung development as well as those involved in aberrant developmental pathology.

Animals↗
PubMed1981

The content of diacylglycerol, triacylglycerol and monoacylglycerol and a comparison of the structural and metabolic heterogeneity of diacylglycerols and phosphatidylcholine during rat lung development.

The content of diacylglycerol in fetal rat lung is approx. 36% of the adult and rapidly increases to adult levels by 1 day after birth. Triacylglycerol content is also low (23%) and increases to adult levels between 1 and 2 days following birth. Monoacylglycerol content is relatively low at all stages of development. The analysis of the molecular species of diacylglycerols showed that the disaturated species accounted for 30-40% of the diacylglycerols and the monoene species 20-28%. Phosphatidylcholine contained 40-45% disaturated and approx. 30% monoene species. The overall pattern of molecular species of phosphatidylcholine was similar to the pattern for diacylglycerol. The in vivo incorporation of [2-3H]glycerol into molecular species of diacylglycerol and phosphatidylcholine in -1-day-fetal (i.e., 1 day before birth) lung showed that the disaturated species of diacylglycerol had the highest incorporation and appeared to have a higher rate of turnover. In contrast, [2-3H]glycerol was incorporated by fetal liver most actively in the monoenoic and dienoic species of diacylglycerol. The relative incorporation of radioactivity into disaturated, monoene and diene species of phosphatidylcholine in fetal lung was very similar to that for the corresponding diacylglycerol species. The rate of the reaction from the disaturated species of diacylglycerol to the disaturated species of phosphatidylcholine, calculated from the in vivo data, was one of the higher rates and indicated considerable potential for the synthesis of disaturated phosphatidylcholine via this route. The overall results suggests that de novo synthesis of disaturated phosphatidylcholine from the disaturated species of diacylglycerol can be a major route for the synthesis of dipalmitoylphosphatidylcholine in fetal lung.

Age Factors↗
PubMedDate not supplied

Differential distribution and increased levels of ras proteins during lung development.

Differential localization of ras proteins and variations in their levels may be of importance during lung growth and differentiation. Abundant cell proliferation occurs during development of the fetal rat lung. As assessed by flow cytometry the proliferative activity declined near birth, followed by a gradual increase in cellular proliferation during the subsequent 8 days and a decline to basal levels by 15 to 18 days of age. During this period of substantial variations in proliferative activity, differences in both the protein content and localization of the different ras proteins were observed. The content of N- and K-ras proteins in lung homogenates increased 5 to 6-fold in rats 20 days or older, compared to fetal levels. The protein levels of the ras proteins remained elevated when cellular proliferation decreased to basal levels. As determined by immunohistochemistry, the localization of N-ras protein was restricted to keratin expressing cells of bronchiolar structures, apparently mainly ciliated cells. In contrast, K-ras was found in alveolar cells, probably type I and type 2 cells. H-ras, but not K- or N-ras, was localized to nonepithelial cells. Thus, different ras proteins were localized to different regions of the lung and increased in abundance during postnatal development.

Animals↗
PubMed2006

Postnatal lung development: immediate-early gene responses post ozone and LPS exposure.

Exposure to environmental pollutants may severely affect lung growth and development. The present study was designed to test the hypothesis that lung damage caused either by ozone or lipopolysaccharide (LPS) occurs through distinct early responses, which are age dependent in the postnatal lung. C57Bl/6 mice ages 4, 10, and 56 days were exposed to inhalation of LPS with an estimated deposited dose of 26 EU and examined 0.5, 1, or 4 h post inhalation exposure; or to 1 or 2.5 ppm ozone for 4 h or sequential exposures of LPS followed by ozone. Abundance of c-fos, c-jun, interleukin (IL)-1beta, Toll-like receptor (TLR) 2, TLR 4, and tumor necrosis factor (TNF) alpha message levels were measured by RNase protection assay. Exposure to ozone for 4 h induced a c-fos and c-jun response in 4-; 10-; and 56-day-old mice in a dose-dependent manner, was localized to conducting and terminal airways, and also induced TLR 4 message abundance in 10- and 56-day-old mice. Exposure to LPS induced c-fos and c-jun 30 and 60 min postinhalation in 10- and 56-day-old mice only. TLR 2 and 4 message abundance was increased at 10 and 56 days, but was undetectable at 4 days of age, and correlated with proinflamatory message induction. Exposure to LPS followed by ozone increased message abundance of IL-1beta, TNFalpha, TLR 2, TLR 4, and c-jun/c-fos at 10 and 56 days, suggesting that combined exposures that induce cellular stresses can regulate gene expression by activating signaling pathways that operate through both transcription factors activator protein (AP)-1 and nuclear factor (NF)-kappaB. However, only c-jun/c-fos and TNFalpha were elevated in 4-day-old mice after sequential exposures, suggesting that the early activation of the inflammatory response after sequential exposures may occur through a TLR-independent pathway. These results suggest that sequential exposures induce multiple signaling pathways that are age dependent.

Air Pollutants↗
PubMed2001

Inadequate lung development and bronchial hyperplasia in mice with a targeted deletion in the Dutt1/Robo1 gene.

Chromosome 3 allele loss in preinvasive bronchial abnormalities and carcinogen-exposed, histologically normal bronchial epithelium indicates that it is an early, possibly the first, somatic genetic change in lung tumor development. Candidate tumor suppressor genes have been isolated from within distinct 3p regions implicated by heterozygous and homozygous allele loss. We have proposed that DUTT1, nested within homozygously deleted regions at 3p12-13, is the tumor suppressor gene that deletion-mapping and tumor suppression assays indicate is located in proximal 3p. The same gene, ROBO1 (accession number ), was independently isolated as the human homologue of the Drosophila gene, Roundabout. The gene, coding for a receptor with a domain structure of the neural-cell adhesion molecule family, is widely expressed and has been implicated in the guidance and migration of axons, myoblasts, and leukocytes in vertebrates. A deleted form of the gene, which mimics a naturally occurring, tumor-associated human homozygous deletion of exon 2 of DUTT1/ROBO1, was introduced into the mouse germ line. Mice homozygous for this targeted mutation, which eliminates the first Ig domain of Dutt1/Robo1, frequently die at birth of respiratory failure because of delayed lung maturation. Lungs from these mice have reduced air spaces and increased mesenchyme, features that are present some days before birth. Survivors acquire extensive bronchial epithelial abnormalities including hyperplasia, providing evidence of a functional relationship between a 3p gene and the development of bronchial abnormalities associated with early lung cancer.

Amino Acid Sequence↗
PubMed1983

Bombesin and vasoactive intestinal polypeptide in the developing lung: marked changes in acute respiratory distress syndrome.

The quantitative distribution of bombesin- and vasoactive intestinal polypeptide (VIP)-like immunoreactivities was determined by RIA and immunocytochemistry in regions of trachea, bronchus, and whole lung at various stages of human fetal development and in neonates, children, and adults. In addition, these two immunoreactivities were studied in infants that had died of the acute respiratory distress syndrome. The concentration of bombesin-like immunoreactivity in the whole respiratory tract steadily increased during gestation, reaching a plateau at birth. In the lung, the bombesin concentration remained almost unchanged during childhood, but decreased to one tenth in the adult. In neonates with the acute respiratory distress syndrome, there was a significantly lower bombesin content in all regions of the respiratory tract compared to either normal full-term infants or 24- to 28-week-old fetuses. Immunocytochemistry localized bombesin immunoreactivity within mucosal neuroendocrine cells present in the airway epithelium throughout the respiratory tract and particularly in the intrapulmonary airways. The number of cells increased throughout gestation, reflecting the pattern found by RIA, and were greatly decreased in acute respiratory distress syndrome patients. VIP concentrations were much lower than those of bombesin and did not change significantly with gestational age. In contrast to bombesin, VIP was mainly concentrated in the upper respiratory tract. In infants with the respiratory distress syndrome, the VIP content was not different from normal. These results are compatible with the possibility that bombesin-like peptides may have a role in the normal development of the human lung.

Acute Disease↗
PubMed1986

Influence of epidermal growth factor on fetal rat lung development in vitro.

Epidermal growth factor (EGF) has been shown to enhance cell multiplication or differentiation in a number of developing tissues. We have examined the effects of this growth factor on the biochemical development of explants of fetal rat lung, cultured in serum-free medium for 48 h. EGF enhanced the rate of choline incorporation into phosphatidylcholine and disaturated phosphatidylcholine in a dose dependent fashion. Half maximal stimulation occurred at a concentration of 1.0 nM, similar to the Kd for EGF binding to rat lung cell membranes. There was also significant stimulation of acetate incorporation into all phospholipids, particularly phosphatidylglycerol (539%), and increased distribution of radioactivity from acetate in this phospholipid fraction. Exposure to EGF stimulated PC synthesis in 18- and 19-day explants (term is 22 days) whereas maximal enhancement of DNA synthesis occurred after this time. This sequence differs from that observed during early embryonic development when EGF initially enhances cell multiplication. An additive interaction with regard to enhancement of PC synthesis was observed with EGF and thyroid hormone, but not EGF and dexamethasone. EGF had no effect on the activity of the enzymes of the choline incorporation pathway of phosphatidylcholine synthesis or on the activity of enzymes involved with acidic phospholipid synthesis. Fetal lung EGF content and EGF binding capacity were not increased by glucocorticoid treatment and similarly glucocorticoid binding capacity was not increased by EGF. These data indicate that EGF enhances fetal rat lung phospholipid synthesis in a dose-dependent manner and suggest that this is a direct effect on the lung tissue mediated by specific receptors.

Animals↗
PubMed1986

Lung development in the streptozotocin rat fetus: antioxidant enzymes and survival in high oxygen.

Offspring of experimentally induced diabetic animals demonstrate delays in functional, biochemical, and morphological aspects of lung maturation, dealing mainly with the surfactant system. To investigate whether the development of the lung antioxidant enzyme system would be similarly delayed, and thus compromise their tolerance to high O2 exposure, we did the following: 1) produced the diabetic state in rats with streptozotocin injection 24 h after the onset of pregnancy; 2) examined fetal animals from streptozotocin and control rats at gestational days 19, 20, and 21, and newborn animals at day 22 for whole lung disaturated phosphatidylcholine and total phospholipid and for the three antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase; and 3) exposed newborn offspring from streptozotocin-treated and control rats to greater than 95% O2 for several days and their survival, changes in antioxidant enzymes and disaturated phosphatidylcholine and light microscopic findings in response to hyperoxic challenge were compared. Streptozotocin offspring demonstrated essentially no developmental differences in whole lung disaturated phosphatidylcholine, total phospholipid, or antioxidant enzymes activity at the 4 gestational days studied. However, newborns of streptozotocin mothers had consistently superior tolerance to hyperoxic exposure, consisting of increased survival [23/34 (68%) versus 8/26 (31%) in controls, after O2-exposure for 13 days, p less than 0.001], microscopic evidence of reduced inhibition of alveolarization (p less than 0.05), and a trend toward greater antioxidant enzymes response. Thus, in this animal model of experimental diabetes, neither the development of the antioxidant enzymes system nor the development of the surfactant system (as assessed by whole lung disaturated phosphatidylcholine and total phospholipid) appear delayed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Effect of antenatal tracheal occlusion on lung development in the sheep model of congenital diaphragmatic hernia: a morphometric analysis of pulmonary structure and maturity.

The incidence of congenital diaphragmatic hernia (CDH) is 1:1,207-5,000, and the condition is associated with high mortality and morbidity, attributed principally to associated pulmonary hypoplasia. Repairing the diaphragmatic defect by antenatal surgery has high mortality, mainly due to premature labor. Antenatal tracheal occlusion, which is achievable by less invasive methods, stimulates lung growth (weight and DNA). However, its effectiveness in reversing structural and maturational abnormalities and its optimal timing requires further investigation. We hypothesized that (1) antenatal tracheal occlusion performed in the lamb model of congenital diaphragmatic hernia will stimulate lung growth and structural development and restore lung structure and maturity toward normal levels by term gestation; (2) effects will be detectable by morphometric measurements of the following parameters: lung volume, ratio of parenchyma to nonparenchyma, volume density of connective tissue within nonparenchyma, ratio of gas exchange tissue to airspace in parenchyma, gas exchange surface area, capillary loading, alveolar/airspace density and alveolar perimeter; (3) effects will be seen in all lobes of the lung; and (4) a greater effect will be observed when tracheal occlusion is performed early rather than late in gestation. Fourteen lambs underwent CDH creation at gestation day 72-74 followed by tracheal occlusion at day 101 (n = 7) or 129 (n = 7). They were delivered by Cesarean section at 143 days (term = 145-149). Lungs were obtained at autopsy, inflation fixed, divided into lobes, and sampled; morphometric analysis was performed. Comparisons were made with previously reported results from control lungs of normal lambs and lambs with untreated CDH. In comparison with untreated lungs, antenatal tracheal occlusion at both times resulted in increased volumes for total lung and lobes, increased volume density of parenchyma and of airspace within parenchyma, and increased gas exchange surface areas. Normal values for gas exchange surface area density, and alveolar density and perimeter were attained and the lungs appeared more mature than non-occluded lungs. Tracheal occlusion earlier in gestation produced a greater effect, achieving greater than normal values for lung volumes and volume densities, whereas the capillary loading value was similar to normal lung. Later occlusion achieved less than normal values for lung volumes and volume densities, with a reduced capillary loading value. We conclude that antenatal tracheal occlusion is capable of reversing structural total lung and lobar hypoplasia and immaturity caused by CDH as determined by morphometrically determined parameters. The effect is greater when tracheal occlusion is performed early rather than late in gestation. The results are encouraging for development of treatment methods for humans with antenatally diagnosed CDH.

Animals↗
PubMed2004

Effects of glucocorticoids on fetal and neonatal lung development.

Antenatal glucocorticoids have been used for 30 years to induce maturation of preterm fetal lungs. Stimulation of the pulmonary surfactant system has been regarded as the most important effect of antenatal glucocorticoids; however, as these drugs alter the expression of a large number of genes they affect the maturation of the lung in several other ways. Antioxidant enzyme production, lung fluid absorption and alveolar development are all affected by glucocorticoids administered in the perinatal period. There is evidence that glucocorticoids induce genes associated with the synthesis of surfactant proteins, fatty acid synthase, the epithelial sodium channel and the membrane protein sodium/potassium ATPase as well as several antioxidant enzymes including catalase, glutathione peroxidase and two superoxide dismutases. Glucocorticoids also increase the expression of vascular endothelial growth factor, which may inhibit alveolarization and lead to abnormally large alveoli. The use of both antenatal and postnatal glucocorticoids has increased in the past decade. However, as concerns about possible long-term effects have arisen, the mechanisms of how glucocorticoids alter the structure and function of the lungs needs to be determined to allow the development of more specific agents in the treatment of respiratory distress syndrome.

Betamethasone↗
PubMed2005

The role of oxygen tension in the regulation of embryonic lung development.

BACKGROUND/PURPOSE: Oxygen tension is an important physiologic mediator of embryonic and fetal development. In vitro studies have demonstrated that the proper embryonic development is dependent upon low oxygen tension and even short exposure to normoxic environments (21%) can be detrimental to embryonic development. We hypothesized that low oxygen tension promotes lung growth in embryonic organ culture and therefore designed this study to investigate embryonic lung growth in normoxic and hypoxic conditions using simple closed chamber. METHODS: Fetal rat lungs were harvested on day 13.5 and placed in organ culture containing serum-free Dulbecco's modified Eagle's medium with antibiotics. The lung cultures were divided into normoxic group, with a 21% oxygen concentration (n = 15), and hypoxic group (n = 15). Hypoxic condition (6% oxygen) was achieved using Oxoid Campygen in a closed chamber. The lungs were placed in 5% carbon dioxide, 37 degrees C incubator for 48 hours. Media were not changed during the incubation period. The morphometric analysis was measured at 0 hour and at 48 hours by counting total terminal buds and entire epithelial contour using Image J software. The fold increase in branching was calculated as the ratio of buds present at 48 hours minus the buds present at 0 hour divided by the number of buds at 0 hour. The increase in entire epithelial contour over 48 hours was calculated in exactly the same way as described above. RESULTS: There was no significant difference in the increase in total terminal buds count in the hypoxic group (2.06 +/- 0.19) compared with the normoxic group (2.59 +/- 0.21), and no significant difference in the increase in entire epithelial contour in the hypoxic group (1.45 +/- 0.11) compared with the normoxic group (1.63 +/- 0.11). CONCLUSIONS: Although hypoxia has been reported to be an important regulator of murine vascular development, our data show that the embryonic lung growth in whole lung organ culture under hypoxic condition is not significantly different from that in normoxic condition.

Animals↗
PubMed1979

Changes in CDP-diglyceride:inositol transferase activity during rabbit lung development.

During fetal and neonatal development the specific activity of the enzyme, CDP-diglyceride:inositol transferase in rabbit lung tissue increased 8- to 9-fold from day 17 of gestation to adulthood. This developmental increase in enzyme activity was not specific for lung tissue since a similar increase was also observed in liver tissue. The properties of CDP-diglyceride:inositol transferase in microsomes prepared from either fetal or adult rabbit lung tissue appeared to be the same. The increase in CDP-diglyceride:inositol transferase activity in rabbit lung tissue during development appeared to be reflective of synthesis of new enzyme rather than activation of pre-existing enzyme.

Animals↗
PubMed1972

Glucocorticoid receptors and the role of glucocorticoids in fetal lung development.

The cellular mechanism of glucocorticoid effects upon fetal lung was examined in studies of specific binding activity for corticosteroids. Cytoplasm of fetal rabbit lung contains receptor sites for [(3)H]dexamethasone at a concentration of 0.43 +/- 0.04 pmol/mg of cytosol protein, and the apparent dissociation constant for the binding reaction is 2.7 +/- 0.4 nM. The ability of various steroids to compete with labeled dexamethasone for binding to receptor correlates with their biologic potency. The hormone-receptor complex formed in vitro at 0 degrees binds with high affinity at 20 degrees to isolated lung nuclei. It is estimated that there are 9500 nuclear binding sites and 12,000 cytoplasmic receptor sites per fetal lung cell. During the last 12 days of gestation in a rabbit, the concentration of cytoplasmic receptor in lung is constant and is 2- to 5-times greater than receptor-site concentration in fetal skin, kidney, heart, muscle, gut, liver, brain, thymus, and placenta. These findings demonstrate that the early steps in the mechanism of glucocorticoid action in target tissues are present in lung cells, and suggest that these hormones accelerate fetal lung differentiation and surfactant production in animals by the induction of new protein synthesis mediated by receptor.

Androgens↗
PubMed1994

Foetal airway motor tone in prenatal lung development of the pig.

The terminal airways from embryonic lung in situ or as explants exhibit rhythmic spontaneous contractions. Our objective was to see whether narrowing responses of the airways occurred throughout the bronchial tree in the first trimester foetus and, if so, to characterize them. The bronchial tree was freed of vasculature and parenchyma from the lungs of 20-35 g pig foetuses (44-48 days gestation). The airway lumen was visualized directly with transmitted light, and narrowing was recorded in real time by video-imaging microscopy. From the main stem bronchi to the terminal regions of late generation branches (20-35 microns i.d.) strong bronchoconstrictor responses to micromolar concentrations of acetylcholine (ACh), histamine, substance P and K+ depolarizing solution were seen, whilst inhibition of narrowing with beta-adrenoceptor agonists was evidence of beta-receptors on the smooth muscle. Moreover, strong narrowing responses to electrical field stimulation, which were blocked by atropine, indicated that functional cholinergic nerves were present. A remarkable display of spontaneous narrowing in the airways of many of the bronchial tree preparations caused the movement of lung liquid to and fro. We speculate that the bronchomotor tone and associated spontaneous activity, which move the lung fluid along the airways, serve to maintain an even positive pressure in localized areas of the bronchial tree which is essential to provide the stimulus for continued growth of the lung.

Acetylcholine↗
PubMed1986

Fetal lung development in male and female nonhuman primates.

Indices of lung maturation were assessed in 58 rhesus fetuses at five gestational ages during the last trimester of nonhuman primate pregnancy to determine whether fetal sex influences lung maturation. In addition to analysis of whole lung phospholipids, glycogen, protein, DNA, and pressure-volume curves surfactant fraction phosphatidylcholine (PC) was quantitated following isolation by sucrose gradient centrifugation and a combination of predictors were assessed by all possible subsets regression to attain a composite "maturity index." For the total population, there was a uniform progression in physical growth characteristics, lung destensibility and stability and phospholipids with advancing gestation. The quantitative change in surfactant fraction PC concentration for both sexes was considerably greater than that observed for whole lung PC between 135 days gestation and term. Further, the increase in surfactant PC occurred in association with improving lung destensibility and deflation stability prior to maximum changes in the whole lung PC or disaturated PC concentration. There were no statistically discernible differences in biochemical or physiological assessment between sexes at any gestational age. These data in nonhuman primates suggest that documented differences in survival from the respiratory distress syndrome between males and females do not result from a discordance in lung maturation as a function of time throughout the last trimester of gestation.

Animals↗
PubMed1995

Effect of zidovudine on human fetal lung development.

Zidovudine (AZT) is currently used to treat human immunodeficiency virus (HIV)-positive women during pregnancy to prevent the prenatal transmission of HIV type 1 (HIV-1). However, AZT not only inhibits HIV replication but also affects the DNA polymerases of human cells; hence AZT is not recommended during the first trimester of pregnancy. The lung is a unique organ because it continues to grow and develop throughout fetal life. Using a human fetal lung organ culture system, we sought to determine the effect of AZT on morphogenesis and epithelial cytodifferentiation of developing alveoli. Lung tissues from three fetuses, 14-15 weeks gestational age, were grown in culture for 24 hours (day 0). AZT at a concentration of either 0.4, 4.0, 8.0, or 40.0 mumol/L was added on days 1, 5, and 10 of growth. The cultures were interrupted on days 6 and 15 and examined by light and electron microscopy for alveolar saccular development, interstitial thinning, and epithelial cell differentiation. On day 6 of growth the treated cultures demonstrated fewer alveolar saccules and a thicker, more cellular interstitium compared to the controls. After 15 days of growth the cultures treated with 0.4 mumol/L of AZT appeared structurally similar to the controls. The cultures treated with AZT concentrations of 4.0 to 40.0 mumol/L appeared unchanged from day 6, implying arrested maturation of the culture. However, epithelial cell differentiation was unaffected. We conclude that AZT at concentrations of 4.0 mumol/L and greater affects the structural development of the human fetal lung in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Differentiation↗
PubMed1992

Chronic in utero beta-blockade alters fetal lung development.

Pregnant rats received propranolol (5 or 10 mg/kg/day) from day 10 of gestation; controls were untreated. Lung wet:dry weight ratios were increased in treated fetuses delivered by hysterotomy at day 21; no difference was seen at birth after vaginal delivery. On subsequent days, treated pups exhibited higher wet:dry weight ratios, implying impaired postnatal lung water clearance. Surfactant pools were decreased proportionately at both doses. Ongoing surfactant synthesis was unaffected at either dose. Baseline secretion was reduced for those exposed to 10 mg/kg/day. Secretory response to beta-agonist stimulation was impaired in both treatment groups. Chronic beta-blockade alters fetal lung water clearance, surfactant stores, and secretory response to beta-agonists.

Abnormalities, Drug-Induced↗
PubMed2001

Pulmonary neuroendocrine cells (PNEC) and neuroepithelial bodies (NEB): chemoreceptors and regulators of lung development.

The airway and alveolar epithelia contain pulmonary neuroendocrine cells whose structure indicates an endocrine function. They are also in contact with sensory nerve fibres. These cells often aggregate into distinct corpuscles-neuroepithelial bodies-and carry membrane receptors sensitive to a number of stimuli, including hypoxia and nicotine. They synthesise, store and release a number of bioactive substances such as serotonin, calcitonin gene-related peptide and the mitogen bombesin. When these are released they contribute to redistribution of pulmonary blood flow, regulation of bronchomotor tone, modulation of the immune response, stimulation of sensory nerve fibres and regulation of lung growth and development. Pulmonary neuroendocrine cells and neuroepithelial bodies seem to be most important in the fetal and neonatal lung as regulators of airway development and hypoxia-sensitive chemoreceptors. There is a link between these cells and specific types of lung cancer and their involvement in lung and paediatric pathology may be profound.

Animals↗