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  • Title: Vascular endothelial growth factor in allergen-induced nasal inflammation.
    Author: Choi GS, Park HJ, Hur GY, Choi SJ, Shin SY, Ye YM, Park HS.
    Journal: Clin Exp Allergy; 2009 May; 39(5):655-61. PubMed ID: 19236408.
    Abstract:
    BACKGROUND: Increased vessel number and permeability are important features of the nasal mucosa in allergic rhinitis (AR), and are mediated in part by the cytokine vascular endothelial growth factor (VEGF). Eosinophils are the major effector cells in the nasal secretions of patients with AR during the responses to allergen challenges. To evaluate the involvement of VEGF in nasal allergic inflammation, we monitored the levels of VEGF, eosinophil cationic protein (ECP), and specific antibodies in the nasal lavage fluids (NLFs) of patients with AR in response to Dermatophagoides pteronyssinus (Dpt). METHODS: Sixty-three subjects with sensitization to Dpt were enrolled: 29 patients with AR (group I) who showed positive responses in a nasal provocation test (NPT) with Dpt; and 34 asymptomatic controls (group II) who showed sensitization to Dpt but negative NPT results. NLF samples were collected at baseline, 10, 30, and 60 min, and at 3, 6, and 24 h during the NPT. The ECP levels in the NLF samples were measured using the ImmunoCAP system. VEGF and Dpt-specific IgE, IgA, and IgG in the NLF samples were detected by ELISA. RESULTS: The eosinophil counts and ECP levels in the samples were significantly increased in group I, but not in group II, during the early and late responses. Although the baseline VEGF level was not significantly different between groups I and II, increased VEGF production was noted in group I after the NPT, especially during the early response. The level of Dpt-specific IgA was significantly increased in group I during the NPT. A relationship was found between the levels of VEGF and ECP or Dpt-specific IgA in the NLF samples collected at 10 min and at 3-6 h (P<0.05, respectively). CONCLUSION: Nasal VEGF secretion in response to allergen exposure may augment eosinophilic inflammation in the nasal mucosa of patients with AR.
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