Increased vascular permeability and endothelial cell growth are important i
n the pathogenesis of otitis media with effusion (OME) and the vascular end
othelial growth factor (VEGF) is known to play an important role in the inc
reased vascular permeability and angiogenesis. To date, at least five isofo
rms of the VEGF family have been identified as VEGF transcripts, encoding p
olypeptides of 206, 189, 165, 145 and 121. but their physiological roles ar
e unclear. The purpose of this study was to investigate the expression of V
EGF, in both endotoxin-induced OME of the rat and human otitis media. We in
stilled endotoxin and saline as a control into the middle ear cavity of the
1 at. Middle ear mucosa were taken at 0 h, 1 h. 3 h, 6 h, 12 h, 1 day, 3 d
ays, 7 days and 14 days and the expression of VEGF mRNA and VEGF protein wa
s evaluated using semi-quantitative RT-PCR and immunohistochemistry. Expres
sion of VEGF164 mRNA and VEGF120 mRNA was first identified 1 h after endoto
xin instillation and was dramatically increased over the period 6 h-l day a
nd then progressively decreased by day 7. The level of expression of VEGF12
0 mRNA was slightly higher than that of VEGF164 mRNA and that of VEGF164 mR
NA was much higher than that of VEGF188 mRNA. Immunostaining revealed expre
ssion of VEGF during 6 h to day 3 and its expression was localized to cilia
ted cells and some inflammatory cells. Wt also pel formed RT-PCRs of cDNA f
rom middle ear fluids of 8 human OME patients and middle ear mucosa of 4 ch
ronic otitis media patients for the identification of VEGF mRNA expression.
VEGF121 mRNA was highly expressed in all samples compared with VEGF165 mRN
A. These results suggest that VEGF may be primarily responsible for increas
ed vascular permeability and endothelial cell growth in OME and that VEGF s
tems to play a significant role in the pathogenesis of OME.