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BDNF and DPP-IV in polyps and middle turbinates epithelial cells
L Jornot1, E Grouzmann, J S Lacroix
1Respiratory Division, Department of Internal Medicine, University Hospitals, Geneva, Switzerland. Lan.H.Jornot@hcuge.ch
Rhinology
|August 22, 2007
Summary
Primary human airway cells produce dipeptidyl peptidase (DPP-IV) and brain-derived neurotrophic factor (BDNF). Pro-inflammatory cytokines increase BDNF production and secretion, indicating its role in airway inflammation.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Neuropeptides contribute to airway inflammation.
- Enzymes like dipeptidyl peptidase (DPP-IV) and neurotrophins like brain-derived neurotrophic factor (BDNF) regulate neuropeptide metabolism in airways.
Purpose of the Study:
- To investigate the expression of DPP-IV and BDNF in primary human nasal epithelial cells.
- To assess the impact of inflammatory conditions on DPP-IV and BDNF levels.
Main Methods:
- Primary human nasal epithelial cells from polyps and turbinates were cultured.
- DPP-IV activity and BDNF expression were measured under basal and inflammatory conditions (TNFα, IL-1β, IFN-γ).
Main Results:
- DPP-IV activity was similar in polyp and turbinate cells.
- Epithelial cells from polyps showed higher BDNF expression than turbinate cells.
- Pro-inflammatory cytokines significantly increased cellular BDNF expression and basolateral secretion, without affecting DPP-IV activity.
Conclusions:
- Primary human airway epithelial cells constitutively produce DPP-IV and BDNF.
- BDNF production and secretion are significantly upregulated by pro-inflammatory cytokines, highlighting BDNF's role in airway inflammation.
