https://orcid.org/0000-0001-5892-2268
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Abstract
Objective
The airway epithelium is a potential source of pathophysiology through activation of transient potential receptor vallinoid type 1 (TRPV1) channel. A positive feedback cycle caused by TRPV1 activity is hypothesized to induce upregulation and production of inflammatory cytokines, leading to exacerbations of chronic airway diseases. These cytokine and protein regulation effects were investigated in this study.
Methods
Healthy (BEAS-2B) and cancer-derived (Calu-3) airway epithelial cell lines were assessed for changes to TRPV1 protein expression and mRNA expression following exposure to capsaicin (5–50 µM), and TRPV1 modulators including heat (43 °C), and hydrochloric acid (pH 3.4 to pH 6.4). Cytotoxicity was measured to determine the working concentration ranges of treatment. Subsequent bronchoconstriction by TRPV1 activation with capsaicin was measured on guinea pig airway tissue to confirm locally mediated activity without the action of known neuronal inputs.
Results
TRPV1 protein expression was not different for all capsaicin, acidity, and heat exposures (p > 0.05), and was replicated in mRNA protein expression (p > 0.05). IL-6 and IL-8 expression were lower in BEAS-2B and Calu-3 cell lines exposed with acidity and heat (p < 0.05), but not consistently with capsaicin exposure, with potential cytotoxic effects possible.
Conclusions
TRPV1 expression was present in airway epithelial cells but its expression was not changed after activation by TRPV1 activators. Thus, it was not apparent the reason for reported TRPV1 upregulation in patients with airway disease states. More complex mechanisms are likely involved and will require further investigation.
Disclosure statement
This research, including all authors, did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Funding
The author(s) reported there is no funding associated with the work featured in this article.