The Laryngoscope · 2025
Laryngeal Basal Cell Response to Cigarette Smoke and E-Cigarette Aerosol Exposures.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Easwaran Meena, Kimura Akari, Liao Hsin-Ying, Khan Mohammed Imran, Golchin Amirbahador, Kiessling Patrick, Erickson-DiRenzo Elizabeth
Аннотация
OBJECTIVE: The laryngeal epithelium contains a basal cell (BC) layer. The BC layer is a reservoir of progenitor cells necessary for the formation and regeneration of the epithelium. The epithelium is susceptible to the deposition of inhaled irritants such as cigarette smoke (CS) and electronic cigarette (E-Cig) aerosol. The objective of this study was to quantify BC, proliferating cells, and epithelial histologic architecture in the larynx following a 6-week exposure to CS or E-Cig aerosol.
METHODS: Mice (N = 12) were assigned to a room-air control, CS-exposed, or an E-Cig-exposed group. Exposures were conducted for 2 h per day, 5 days a week for a total of 6 weeks. Mice were then euthanized and the larynx was evaluated using immunofluorescence and histology. We assessed p63-positive BCs, Ki67-positive proliferating cells, p63 and Ki67 colocalized cells, overall cellularity, and epithelial thickness across the supraglottic, vocal fold, and subglottic regions of the larynx.
RESULTS: Following E-Cig exposure, there was a significant reduction in p63-positive BC in the vocal folds as compared to the CS-exposed and control group and epithelial thickness compared to the CS-exposed group. No significant changes were observed in the numbers of BCs, proliferating cells, colocalized cells, or overall cellularity in any of the other laryngeal regions examined.
CONCLUSION: An E-Cig-induced reduction in BCs within the vocal fold epithelium may have implications for decreased regenerative capacity. Overall, our findings highlight distinct epithelial responses to CS and E-Cig exposures and underscore the regional heterogeneity of the laryngeal response to these common inhaled challenges.
METHODS: Mice (N = 12) were assigned to a room-air control, CS-exposed, or an E-Cig-exposed group. Exposures were conducted for 2 h per day, 5 days a week for a total of 6 weeks. Mice were then euthanized and the larynx was evaluated using immunofluorescence and histology. We assessed p63-positive BCs, Ki67-positive proliferating cells, p63 and Ki67 colocalized cells, overall cellularity, and epithelial thickness across the supraglottic, vocal fold, and subglottic regions of the larynx.
RESULTS: Following E-Cig exposure, there was a significant reduction in p63-positive BC in the vocal folds as compared to the CS-exposed and control group and epithelial thickness compared to the CS-exposed group. No significant changes were observed in the numbers of BCs, proliferating cells, colocalized cells, or overall cellularity in any of the other laryngeal regions examined.
CONCLUSION: An E-Cig-induced reduction in BCs within the vocal fold epithelium may have implications for decreased regenerative capacity. Overall, our findings highlight distinct epithelial responses to CS and E-Cig exposures and underscore the regional heterogeneity of the laryngeal response to these common inhaled challenges.