ACHEMS 2019
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SPLTRAK Abstract Submission
Exposure to IL-13 Increases Number of Solitary Chemosensory Cell Markers in Primary Nasal Epithelial Air-Liquid Interface Cultures
Shivani Pathak1,2,3,4, Eric Larson1,2,3,4, Catherine Anderson1,2,3,4, Vijay Ramakrishnan1,2,3,4
1Rocky Mountain Smell and Taste Center, Aurora, CO, United States
2Department of Otolaryngology, Aurora, CO, United States
3Department of Developmental and Cell Biology, Aurora, CO, United States
4University of Colorado School of Medicine, Aurora, CO, United States

Cellular differentiation towards a committed cytotype within the nasal epithelium can go in one of two directions: either towards a secretory or a ciliated cell fate. Solitary chemosensory cells (SCCs) are secretory cells that proliferate throughout the life of the adult animal, similar to the replacement rate of other sensory cells, namely the olfactory sensory neurons and taste cells. These sensory cells originate from basal cells within the epithelial lining that express particular transcription factors. Prior research has shown that SCC activation by bitter compounds or bacterial metabolites triggers trigeminal nerve stimulation resulting in cardinal signs of nasal inflammation including plasma extravasation and mast cell degranulation. SCCs have demonstrated importance in type 2 inflammation, where the chemokine IL-13 is known to induce goblet cell hyperplasia and decreased ciliation. We hypothesize that IL-13 exposure results in SCC proliferation in differentiated cell culture, consistent with its known effect on driving secretory cell fate. We exposed primary human nasal epithelial air-liquid interface (ALI) cultures to IL-13 at 20ng/mL for 2 weeks post differentiation and collected RNA for qualitative polymerase chain reaction. Our results reveal an increase in expression of the SCC markers alpha-gustducin and transient receptor potential cation channel subfamily M member 5 in the exposed group. Similar to previously published data, we also find a decrease in expression of the ciliated cell marker ARL13 and an increase in expression of the goblet cell marker MUC5B. This finding suggests that IL-13 exposure drives differentiation of the airway epithelium towards a secretory cell fate and increases the number of SCCs within the epithelial culture unit.