scholarly journals Innervation of Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Developing Rabbit Lung

2004 ◽  
Vol 52 (3) ◽  
pp. 379-389 ◽  
Author(s):  
Jie Pan ◽  
Herman Yeger ◽  
Ernest Cutz
PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy

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.


2019 ◽  
Vol 19 (1S) ◽  
pp. 43-44
Author(s):  
M A Syrczova ◽  
D E Korzhevskii

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.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ling Cai ◽  
Hongyu Liu ◽  
Fang Huang ◽  
Junya Fujimoto ◽  
Luc Girard ◽  
...  

AbstractSmall cell lung cancer (SCLC) is classified as a high-grade neuroendocrine (NE) tumor, but a subset of SCLC has been termed “variant” due to the loss of NE characteristics. In this study, we computed NE scores for patient-derived SCLC cell lines and xenografts, as well as human tumors. We aligned NE properties with transcription factor-defined molecular subtypes. Then we investigated the different immune phenotypes associated with high and low NE scores. We found repression of immune response genes as a shared feature between classic SCLC and pulmonary neuroendocrine cells of the healthy lung. With loss of NE fate, variant SCLC tumors regain cell-autonomous immune gene expression and exhibit higher tumor-immune interactions. Pan-cancer analysis revealed this NE lineage-specific immune phenotype in other cancers. Additionally, we observed MHC I re-expression in SCLC upon development of chemoresistance. These findings may help guide the design of treatment regimens in SCLC.


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