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

2001 ◽  
Vol 2 (2) ◽  
pp. 171-176 ◽  
Author(s):  
A.Van Lommel
Keyword(s):  
Lung Development ◽  
Neuroendocrine Cells ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells

Maternal Smoking and Pulmonary Neuroendocrine Cells in Sudden Infant Death Syndrome

PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Airway Epithelium ◽  
Maternal Smoking ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Sudden Infant ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells

Background. Maternal smoking is a well-recognized risk factor for sudden infant death syndrome (SIDS), but the precise mechanism is unknown. We tested a hypothesis that maternal smoking affects pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs), which are innervated PNEC clusters and presumed airway chemoreceptors. Methods. Lung sections from infants who died of SIDS and whose mothers smoked during pregnancy (n = 22), infants who died of SIDS and whose mothers were nonsmokers (n = 17), and age-matched control infants (n = 15) who died of other causes were immunostained for bombesin (a PNEC and NEB marker) and assessed morphometrically. Results. The frequency of PNEC (the percentage of airway epithelium immunoreactive for bombesin) was increased up to twofold in the lungs of infants who died of SIDS (7.7 ± 0.4%) compared with controls (4.9 ± 0.4%), as was the frequency (40 ± 3.5 vs 23 ± 3.7/cm2) and size (748 ± 46.5 vs 491 ± 25.8,µm2) of NEBs. In infants who died of SIDS and who were born to smoking mothers, PNEC frequency was increased significantly compared with that in those born to nonsmoking mothers, but the frequency and size of NEBs were not significantly different between the two groups. Conclusion. Our findings suggest that maternal smoking potentiates hyperplasia of the PNEC system in the lungs of infants who die of SIDS and that a dysfunction of these cells may contribute to the pathophysiology of SIDS.

scholarly journals Mechanical stretch-induced serotonin release from pulmonary neuroendocrine cells: implications for lung development

2006 ◽  
Vol 290 (1) ◽  
pp. L185-L193 ◽  
Author(s):  
Jie Pan ◽  
Ian Copland ◽  
Martin Post ◽  
Herman Yeger ◽  
Ernest Cutz
Keyword(s):  
Lung Development ◽  
Tryptophan Hydroxylase ◽  
Mechanical Strain ◽  
Fetal Lung ◽  
Mechanical Stretch ◽  
Serotonin Release ◽  
Neuroendocrine Cells ◽  
Cyclic Stretch ◽  
Mechanosensitive Channels ◽  
Pulmonary Neuroendocrine Cells

Pulmonary neuroendocrine cells (PNEC) produce amine (serotonin, 5-HT) and peptides (e.g., bombesin, calcitonin) with growth factor-like properties and are thought to play an important role in lung development. Because physical forces are essential for lung growth and development, we investigated the effects of mechanical strain on 5-HT release in PNEC freshly isolated from rabbit fetal lung and in the PNEC-related tumor H727 cell line. Cultures exposed to sinusoidal cyclic stretch showed a significant 5-HT release inhibitable with gadolinium chloride (10 nM), a blocker of mechanosensitive channels. In contrast to hypoxia (Po2 ∼ 20 mmHg), stretch-induced 5-HT release was not affected by Ca2+-free medium or nifedipine (50 μM), excluding the exocytic pathway. In H727 cells, stretch failed to release calcitonin, a peptide stored within dense core vesicles (DCV), whereas hypoxia caused massive calcitonin release. 5-HT released by mechanical stretch is derived predominantly from the cytoplasmic pool, because it is rapid (∼5 min) and is releasable from early (20 days of gestation) fetal PNEC containing few DCV. Both mechanical stretch and hypoxia upregulated expression of tryptophan hydroxylase, the rate-limiting enzyme of 5-HT synthesis. We conclude that mechanical strain is an important physiological stimulus for the release of 5-HT from PNEC via mechanosensitive channels with potential effects on lung development and resorption of lung fluid at the time of birth.

scholarly journals NEUROEPITHELIAL BODIES OF THE RAT’S LUNGS IN EXPERIMENTAL ASTHMA

2019 ◽  
Vol 19 (1S) ◽  
pp. 43-44
Author(s):  
M A Syrczova ◽  
D E Korzhevskii
Keyword(s):  
Single Cells ◽  
Neuroendocrine Cells ◽  
Biologically Active ◽  
Medium Size ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells ◽  
Functional Features ◽  
Large Clusters ◽  
Sexually Mature ◽  
Active Substances

The epithelium of the respiratory tract of mammalian lungs contains pulmonary neuroendocrine cells, represented by both single cells and innervated clusters forming neuroepithelial bodies (NEB). Since NEB are intensively innervated and produce highly specific biologically active substances, such as the bronchoconstrictor serotonin, the level of which increases during hypoxia, it is assumed that these structures can play a key role in the pathogenesis of bronchial asthma (BA).The purpose of this study was to the detection and analysis of NEB in the lungs with experimental BA.For the study, we used the lungs of sexually mature Wistar rats (n = 5). NEB was detected by monoclonal antibodies to synaptophysine.It has been found but that in the context of experimental asthma 76.6% NEB were located as part of a simple cuboidal epithelium of small bronchi and respiratory bronchioles. 17.6% of NEB were found in the composition of the epithelial layer and only 5.8% are single NEB in the composition of the epithelium of the small bronchi. At the same time, a greater number of NEB localized in the bronchi were composed of 6 cells (46.2%), 38.5% of 4 cells, and 15.3% of more than 10 cells in one cluster. As in our previous studies, most of the NEB were located in the vicinity of the synaptophysi-immunopositive terminals. Against the background of asthma occurred reduction in the number of large clusters NEB and increased concentrations of medium size of NEB. The results obtained indicate the effect of inflammation on the functional features of the neuroendocrine system of the lungs and the possible contribution of NEB to the inflammatory cascade in BA.

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