PMID- 12220474
OWN - NLM
STAT- MEDLINE
DCOM- 20030306
LR  - 20190901
IS  - 0954-7894 (Print)
IS  - 0954-7894 (Linking)
VI  - 32
IP  - 9
DP  - 2002 Sep
TI  - Activation of the specific neurotrophin receptors TrkA, TrkB and TrkC influences 
      the function of eosinophils.
PG  - 1348-54
AB  - BACKGROUND: Recent studies have shown that nerve growth factor (NGF) can act on 
      several immune cells as well as residential cells. But little is known about 
      their role in modulating eosinophil function via activation of high-affinity 
      receptors. OBJECTIVES: The aim of this study was to assess whether eosinophils 
      express functional receptors and if their function is influenced by NGF, 
      brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). METHODS: 
      Eosinophils were purified by negative immunoselection (purity > 96%). 
      High-affinity neurotrophin receptors were demonstrated by reverse transcription 
      polymerase chain reaction, western blotting and flow-cytometry analysis. 
      Functionality of receptors was demonstrated by receptor phosphorylation after 
      ligand binding. Eosinophils were incubated with NGF, BDNF and NT-3, and cells and 
      supernatants were collected for measurement of the mediators IL-4, IL-5, IL-8, 
      transforming growth factor (TGF)-beta1, eosinophil cationic protein (ECP), 
      eosinophil protein X (EPX) as well as eosinophil viability. RESULTS: Eosinophils 
      expressed mRNA for neurotrophin receptors. Proteins were detectable by western 
      blot and fluorescent-activated cell sorter analysis. The receptors were 
      phosphorylated after stimulation with neurotrophins. After NGF stimulation, a 
      significant increase in IL-4 was detectable. BDNF and NT-3 stimulation led to a 
      significant increase in EPX. Eosinophil viability was not influenced. 
      CONCLUSIONS: Eosinophils express the functionally active receptors TrkA, TrkB and 
      TrkC. Receptor activation stimulates eosinophils. This might be an additional 
      pathway regulating inflammatory responses in allergic reactions.
FAU - Noga, O
AU  - Noga O
AD  - Allergy and Asthma Clinic, Charite, Campus Virchow, Humboldt University, Berlin, 
      Germany. oliver.noga@charite.de
FAU - Englmann, C
AU  - Englmann C
FAU - Hanf, G
AU  - Hanf G
FAU - Grutzkau, A
AU  - Grutzkau A
FAU - Guhl, S
AU  - Guhl S
FAU - Kunkel, G
AU  - Kunkel G
LA  - eng
PT  - Journal Article
PL  - England
TA  - Clin Exp Allergy
JT  - Clinical and experimental allergy : journal of the British Society for Allergy 
      and Clinical Immunology
JID - 8906443
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neurotrophin 3)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (Receptor, trkC)
SB  - IM
CIN - Clin Exp Allergy. 2002 Sep;32(9):1266-8. PMID: 12220461
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Eosinophils/*metabolism
MH  - Flow Cytometry
MH  - Humans
MH  - Inflammation Mediators/analysis
MH  - Nerve Growth Factors/*pharmacology
MH  - Neurotrophin 3/pharmacology
MH  - Phosphorylation
MH  - RNA, Messenger/analysis
MH  - Receptor, trkA/genetics/metabolism
MH  - Receptor, trkB/genetics/metabolism
MH  - Receptor, trkC/genetics/metabolism
MH  - Receptors, Nerve Growth Factor/genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Rhinitis, Allergic, Perennial/*immunology
MH  - Statistics, Nonparametric
EDAT- 2002/09/11 10:00
MHDA- 2003/03/07 04:00
CRDT- 2002/09/11 10:00
PHST- 2002/09/11 10:00 [pubmed]
PHST- 2003/03/07 04:00 [medline]
PHST- 2002/09/11 10:00 [entrez]
AID - 1442 [pii]
AID - 10.1046/j.1365-2745.2002.01442.x [doi]
PST - ppublish
SO  - Clin Exp Allergy. 2002 Sep;32(9):1348-54. doi: 10.1046/j.1365-2745.2002.01442.x.