Pulmonary Neuroendocrine cells and Neuroepithelial bodies in Sudden Infant Death Syndrome: Potential markers of airway chemoreceptor dysfunction

2006 ◽  
Vol preprint (2007) ◽  
pp. 1
Author(s):  
Ernest Cutz ◽  
Donald Perrin ◽  
Jie Pan ◽  
Elizabeth Hass ◽  
Henry Krous
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Sudden Infant ◽  
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.

Abnormal Patterns of Pulmonary Neuroendocrine Cells in Victims of Sudden Infant Death Syndrome

PEDIATRICS ◽  
1989 ◽  
Vol 84 (5) ◽  
pp. 828-834
Author(s):  
John E. Gillan ◽  
Carmel Curran ◽  
Eileen O'Reilly ◽  
Seamus F. Cahalane ◽  
Anthony R. Unwin
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Chronic Hypoxia ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Neuroendocrine Cell ◽  
Sudden Infant ◽  
Pulmonary Neuroendocrine Cells ◽  
Structural Abnormalities ◽  
Brainstem Dysfunction

Ventilatory dysfunction has become the main focus of current research in sudden infant death syndrome (SIDS). This has been correlated with structural abnormalities in the carotid body and respiratory nuclei of the brainstem. In recent studies, the denervating effect of asphyxial brainstem dysfunction on the pulmonary neuroendocrine cells, which probably function as chemoreceptors, was demonstrated and prompted the following study. The pulmonary neuroendocrine system was evaluated in 25 victims of SIDS and 20 control infants, ranging in age from 3 weeks to 7 months and 1 to 12 months, respectively. The pulmonary neuroendocrine cells were stained by the Churukian-Schenk method and the neuroendocrine cell-positive airway values expressed as a percentage of the total number of airways. The range of positive airway values for victims of SIDS was 2% to 97% with a median of 73%. In contrast, the range for the control infants was 1% to 44% with a median of 25.5%. The SIDS victims' percentage was significantly greater than the control infants' percentage (P< .0001). The number of pulmonary neuroendocrine cells in positive airway was also increased among SIDS victims compared with control infants. The altered plumonary neuroendocrine cell pattern could be attributable to either brainstem dysfunction or chronic hypoxia. These explanations are not, however, mutually exclusive of one another; in fact, it is possible that both mechanisms may be operative.

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