Abstract
Purpose:
Age-related macular disease (AMD) is one of the leading causes of blindness in the west world with choroidal neovascularization (CNV) accounting for 20% of the cases. Until now the exact mechanisms for choroidal neovascularization are not well understood and treatment has been focused toward anti-VEGF therapy with poor visual outcomes. Takeda et al published that blockade of CCR3/CCL11 in animal models inhibit CNV. We hypothesize that blood expression of CCL11 could be present in patients with retinal and CNV.
Methods:
A case control study that included 64 patients with AMD (23) , proliferative diabetic retinopathy (20) and healthy patients (21). 1) AMD: patients older than 50 y.o. with an active CNV confirmed with clinical evaluation, leakage in retinal angiography and subretinal or intraretinal fluid by OCT. 2) PDR: Older than 50 years old with retinal neovascularization secondary to PDR without any clinical feature of AMD. 3) Healthy patients: Older than 50 y.o. without diabetes mellitus (fasting glucose <126 mg/dl) and any clinical feature of AMD or diabetic retinopathy. Exclusion criteria: history of inflammatory conditions, use of steroidal anti-inflammatory or immune-modulating agents, history of cancer, liver disease, vascular diseases, blood dyscrasias and recent surgery (<120 days). A fasting blood sample was obtained in all the patients and determination of CCL11 by ELISA was performed.
Results:
An ANOVA test showed that CCL11 was significantly increased in patients with AMD (p<0.05) in comparison with the other 2 groups. A linear regression analysis comparing age and serum levels of CCL11 in the 3 groups showed no statistically significant difference (p>0.05) ruling out any association between the higher levels of CCL11 and the higher age average in AMD group. A t-student test comparing the gender and CCL11 levels in the three groups ruled out any association between higher CCL11 levels and the higher number of females in the AMD group (p>0.05).
Conclusions:
Blood expression of CCL11 is present in patients with active CNV. The blockade of the complex CCR3/CCL11 could represent a therapeutic option in patients with CNV. Further studies are required to determine the intraocular expression of CCL11 in AMD and to better understand the CCR3/CCL11 choroidal neovascularization pathwaya in humans with exudative AMD.