PMID- 17708459
OWN - NLM
STAT- MEDLINE
DCOM- 20071206
LR  - 20101118
IS  - 0300-0729 (Print)
IS  - 0300-0729 (Linking)
VI  - 45
IP  - 2
DP  - 2007 Jun
TI  - BDNF and DPP-IV in polyps and middle turbinates epithelial cells.
PG  - 129-33
AB  - HYPOTHESIS: Neuropeptides released from sensory nerves may contribute to airway 
      inflammation, particularly if their metabolism is impaired through defective 
      inactivation and/or increased production. In the airways, neuropeptides are 
      subjected to degradation by enzymes such as dipeptidyl peptidase (DPP-IV), and 
      are upregulated by neurotrophins such as brain derived neurotrophic factor 
      (BDNF). We therefore assessed in primary human nasal epithelial cells the 
      expression of DPP-IV and BDNF under basal and inflammatory conditions. METHODS: 
      Human epithelial cells were isolated from nasal polyps and middle turbinates, and 
      grown on collagen-coated polycarbonate filters with an air liquid-interface. 
      After three weeks of culture, constitutive cellular expression of DPP-IV and BDNF 
      was assessed by measuring its activity and by ELISA, respectively. To mimick in 
      vivo inflammatory conditions, cells were exposed apically and basolaterally to 50 
      ng/ml of TNFalpha, IL-1beta, and IFN-gamma for two days. DPP-IV activity and BDNF 
      protein expression were measured in cell lysates and in the apical and 
      basolateral media. RESULTS: Constitutive DPP-IV activity was similar in polyps 
      and turbinates cells. In contrast, polyps epithelial cells expressed higher 
      amounts of BDNF compared to turbinates derived cells. On the other hand, 
      TNFalpha, IL-1beta, and IFN-gamma did not affect DPP-IV activity but 
      significantly increased the cellular expression and the basolateral secretion of 
      BDNF. CONCLUSIONS: Our data show for the first time that primary human airway 
      epithelial cells produced DPP-IV and BDNF under basal conditions. Furthermore, 
      the production and secretion of BDNF were markedly increased in response to 
      pro-inflammatory cytokines, confirming the involvement of BDNF in airway 
      inflammation.
FAU - Jornot, L
AU  - Jornot L
AD  - Respiratory Division, Department of Internal Medicine, University Hospitals, 
      Geneva, Switzerland. Lan.H.Jornot@hcuge.ch
FAU - Grouzmann, E
AU  - Grouzmann E
FAU - Lacroix, J S
AU  - Lacroix JS
FAU - Rochat, T
AU  - Rochat T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Rhinology
JT  - Rhinology
JID - 0347242
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 3.4.14.5 (DPP4 protein, human)
RN  - EC 3.4.14.5 (Dipeptidyl Peptidase 4)
SB  - IM
MH  - Brain-Derived Neurotrophic Factor/analysis/*biosynthesis
MH  - Cells, Cultured
MH  - Dipeptidyl Peptidase 4/analysis/*biosynthesis
MH  - Epithelial Cells/chemistry/*metabolism
MH  - Humans
MH  - Nasal Cavity/*cytology
MH  - Nasal Polyps/chemistry/*metabolism
MH  - Turbinates
EDAT- 2007/08/22 09:00
MHDA- 2007/12/07 09:00
CRDT- 2007/08/22 09:00
PHST- 2007/08/22 09:00 [pubmed]
PHST- 2007/12/07 09:00 [medline]
PHST- 2007/08/22 09:00 [entrez]
PST - ppublish
SO  - Rhinology. 2007 Jun;45(2):129-33.