PMID- 12794063
OWN - NLM
STAT- MEDLINE
DCOM- 20030707
LR  - 20190616
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 992
DP  - 2003 May
TI  - Neurotrophins in allergic airway dysfunction: what the mouse model is teaching 
      us.
PG  - 241-9
AB  - Neurotrophins such as nerve growth factor (NGF) and brain-derived neurotrophic 
      factor (BDNF) are potent mediators of neuronal plasticity in the adult. There is 
      increasing evidence that they regulate a variety of immune functions as well. 
      Thus, neurotrophins are candidate molecules for neuroimmune interactions in 
      allergic bronchial asthma, where elevated neurotrophin levels have been reported. 
      In a mouse model of allergic airway inflammation we have identified macrophages 
      and lymphocytes as additional cellular sources of NGF and BDNF in the inflamed 
      lung. There was an unusual time course of BDNF in bronchoalveolar lavage fluid. 
      BDNF levels peaked 1 week after the last allergen challenge, and did not 
      correlate with the time course of the inflammatory response. In a series of 
      experiments using blocking anti-NGF and anti-BDNF antibodies, we have shown that 
      NGF specifically enhances inflammation and the allergic early-phase response. In 
      contrast, BDNF influenced chronic airway obstruction and local neuronal 
      hyperreactivity without affecting inflammation. Using transgenic mice 
      overexpressing NGF in the airway epithelium, we have confirmed the data obtained 
      from anti-NGF experiments. Allergen-challenged NGF overexpressors displayed a 
      markedly augmented airway inflammation, early-phase response, and sensory 
      irritation compared to wild-type mice. Studies with p75-NTR (-/-) knockout mice 
      showed that these NGF effects are at least in part mediated by the low-affinity 
      neurotrophin receptor. Thus, our experiments suggest that NGF and BDNF have a 
      profound, but differential impact on allergic airway dysfunction.
FAU - Lommatzsch, Marek
AU  - Lommatzsch M
AD  - Department of Pneumology, University of Rostock, 18055 Rostock, Germany. 
      marek.lommatzschmed.uni-rostock.de
FAU - Braun, Armin
AU  - Braun A
FAU - Renz, Harald
AU  - Renz H
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Allergens)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Allergens
MH  - Animals
MH  - Asthma/physiopathology
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Disease Models, Animal
MH  - Humans
MH  - Hypersensitivity/immunology/*physiopathology
MH  - Inflammation/physiopathology
MH  - Mice
MH  - Nerve Growth Factors/immunology/*physiology
MH  - Neuronal Plasticity/physiology
RF  - 44
EDAT- 2003/06/10 05:00
MHDA- 2003/07/08 05:00
CRDT- 2003/06/10 05:00
PHST- 2003/06/10 05:00 [pubmed]
PHST- 2003/07/08 05:00 [medline]
PHST- 2003/06/10 05:00 [entrez]
AID - 10.1111/j.1749-6632.2003.tb03154.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2003 May;992:241-9. doi: 10.1111/j.1749-6632.2003.tb03154.x.