Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Sudden Infant Death Syndrome: Potential Markers of Airway Chemoreceptor Dysfunction

• DOI: 10.2350/06-06-0113.1
• Publication Date: 2007-03-07T14:35:55Z
• Authors: Ernest Cutz; Donald G. Perrin; Jie Pan; Elisabeth A. Haas; Henry F. Krous
• Keywords: Sudden Death; Hypoxia; Decompensation

Pulmonary neuroendocrine cells (PNEC), including neuroepithelial bodies (NEB), are amine- and peptide (for example, bombesin)–producing that function as hypoxia/hypercapnia-sensitive chemoreceptors could be involved in the pathophysiology of sudden infant death syndrome (SIDS). We assessed morphometrically frequency size PNEC/NEB lungs infants who died SIDS ( n = 21) compared them to an equal number age-matched control accidental or homicide, with all cases obtained from San Diego SIDS/SUDC Research Project database. As a marker for we used antibody against chromogranin A (CGA), computer-assisted morphometric analysis was employed determine relative PNEC per airway epithelial area (% immunostained area, %IMS), NEB, nuclei/NEB, NEB cells. The showed significantly greater %IMS epithelium (2.72 ± 0.28 [standard error mean, SEM] versus 1.88 0.24; P < 0.05) larger (1557 153 μm 2 1151 106 ; infants. also increased controls (180 6.39 157 8.0 0.05), indicating presence hypertrophy addition hyperplasia. Our findings support previous studies demonstrating hyperplasia SIDS. These changes secondary chronic hypoxia and/or attributable maturational delay. Morphometric assessment measurement secretory products these CGA, bombesin) provide potential biological