PMID- 18266897 OWN - NLM STAT- MEDLINE DCOM- 20080415 LR - 20151119 IS - 1398-9995 (Electronic) IS - 0105-4538 (Linking) VI - 63 IP - 4 DP - 2008 Apr TI - Modulation of neurotrophin and neurotrophin receptor expression in nasal mucosa after nasal allergen provocation in allergic rhinitis. PG - 468-75 LID - 10.1111/j.1398-9995.2008.01626.x [doi] AB - BACKGROUND: Patients with allergic rhinitis (AR) feature both allergic airway inflammation and a hyperresponsiveness to nonspecific stimuli which is partly neuronally controlled. Still, it is unclear whether or not neurotrophins are involved in airway pathophysiology of AR and in nasobronchial interaction. METHODS: Nine AR patients with mono-allergy to grass pollen and nine healthy controls underwent nasal allergen provocation (NP). Serum samples, nasal and bronchial biopsies were taken before (T(0)) and 24 h after (T(24)) NP. Pan-neurotrophin receptor p75(NTR), tyrosine kinase A (trkA), trkB, nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) were assessed with immunohistochemistry, and NGF and BDNF levels with ELISA. RESULTS: At T(24), BDNF and NGF were upregulated in nasal mucosa (P < 0.05) and increased in the peripheral blood of AR compared with T(0). The increase in nasal BDNF expression correlated positively with the maximum increase in total nasal symptom score in AR (P = 0.02). p75(NTR) was expressed on peripheral nerves and epithelial layer, trkA on endothelial cells, and trkB on mast cells. trkB + mast cells significantly decreased after NP in AR (P < 0.01). NP did not modulate p75(NTR) and trkA expression in nasal mucosa and had no effect on the expression of neurotrophins and receptors in bronchial mucosa. CONCLUSION: This study shows that neurotrophins and their receptors are expressed in human airways. Allergic rhinitis was characterized by a modulation of BDNF, NGF, and trkB in nasal mucosa after NP and a correlation of nasal BDNF with the maximal increase of total nasal symptom score. Therefore, our data suggest that neurotrophins participate in upper-airway pathophysiology in AR, whereas their role in nasobronchial interaction remains unclear. FAU - Raap, U AU - Raap U AD - Department of Dermatology and Allergology, Hannover Medical University, Hannover, Germany. FAU - Fokkens, W AU - Fokkens W FAU - Bruder, M AU - Bruder M FAU - Hoogsteden, H AU - Hoogsteden H FAU - Kapp, A AU - Kapp A FAU - Braunstahl, G-J AU - Braunstahl GJ LA - eng PT - Clinical Trial PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20080211 PL - Denmark TA - Allergy JT - Allergy JID - 7804028 RN - 0 (Allergens) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Receptor, Nerve Growth Factor) RN - 9061-61-4 (Nerve Growth Factor) RN - EC 2.7.10.1 (Receptor, trkA) RN - EC 2.7.10.1 (Receptor, trkB) SB - IM MH - Adult MH - Allergens MH - Brain-Derived Neurotrophic Factor/blood/*immunology MH - Bronchi/immunology MH - Female MH - Humans MH - Male MH - Mast Cells/immunology MH - Nasal Cavity/immunology MH - Nasal Provocation Tests MH - Nerve Growth Factor/blood/*immunology MH - Poaceae/immunology MH - Pollen/immunology MH - Receptor, Nerve Growth Factor/*immunology MH - Receptor, trkA/*immunology MH - Receptor, trkB/*immunology MH - Respiratory Mucosa/*immunology MH - Rhinitis, Allergic, Seasonal/blood/*immunology EDAT- 2008/02/13 09:00 MHDA- 2008/04/16 09:00 CRDT- 2008/02/13 09:00 PHST- 2008/02/13 09:00 [pubmed] PHST- 2008/04/16 09:00 [medline] PHST- 2008/02/13 09:00 [entrez] AID - ALL1626 [pii] AID - 10.1111/j.1398-9995.2008.01626.x [doi] PST - ppublish SO - Allergy. 2008 Apr;63(4):468-75. doi: 10.1111/j.1398-9995.2008.01626.x. Epub 2008 Feb 11.