Experimental Eye Research 138 (2015) 124e125

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Letter to the Editor

Comment on ‘Caffeic acid phenethyl ester lessens disease symptoms in an experimental autoimmune uveoretinitis mouse model’ by Choi J.H. et al. [Exp. Eye Res. 134 (2015) 53e62] Haci Kemal Erdemli a, Sumeyya Akyol b, *, Ferah Armutcu c, Omer Akyol d a

Department of Biochemistry Laboratory, Corum Training and Research Hospital, Corum, Turkey Department of Medical Biology, Faculty of Medicine, Turgut Ozal University, Ankara, Turkey Department of Medical Biochemistry, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey d Department of Medical Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, Turkey b c

a r t i c l e i n f o Article history: Received 30 June 2015 Received in revised form 7 July 2015 Accepted in revised form 8 July 2015 Available online 10 July 2015

Dear Editor, We read with interest the original article entitled ‘Caffeic acid phenethyl ester lessens disease symptoms in an experimental autoimmune uveoretinitis mouse model’ (Choi et al., 2015, Exp. Eye Res. 134, 53e62). The authors have pointed out that caffeic acid phenethyl ester (CAPE) is a potential therapeutic agent for autoimmune uveoretinitis (EAU), a prevalent Th-1-mediated autoimmune disease, that acts by inhibiting cellular infiltration into the retina, reducing the levels of pro-inflammatory cytokines, chemokines, and interphotoreceptor retinal-binding protein-specific antibody and blocking NFkB pathway activation. Having gone through the article, we would like to add the following points. Limited literature is available regarding the beneficial effects of CAPE on major eye diseases, most of which are related to cataract, corneal diseases, and posterior capsule opacification (PCO). The first study about the effect of CAPE regarding bovine lens was about the relationship between oxidative stress and the protection by CAPE (Frenkel et al., 1993, Cancer Res, 53, 1255e61). They found that 12-O-tetradecanoylphorbol-13-acetate-induced H2O2 production in bovine lenses was inhibited by CAPE. It was followed by an experimental study (Hepsen et al., 1997, J Cataract Refratc Surg, 23,

DOI of original article: http://dx.doi.org/10.1016/j.exer.2015.03.014. * Corresponding author. Turgut Ozal University, Faculty of Medicine, Department of Medical Biology, Camlica Mh. Anadolu Bulv. No: 16/A, Gimat, Yenimahalle, Ankara, Turkey. E-mail address: [email protected] (S. Akyol). http://dx.doi.org/10.1016/j.exer.2015.07.003 0014-4835/© 2015 Elsevier Ltd. All rights reserved.

1572e1576) suggesting that PCO in pigmented rabbits had been suppressed by CAPE. To the best of our knowledge, there is only one report that has described the protective effects of CAPE on EAU, which is the paper by Choi et al. (2015) on which we are commenting. It is indeed noteworthy that the authors of this article have taken research with CAPE to the protection of the symptoms of another autoimmune disorder (experimental allergic encephalomyelitis (EAE)-induced oxidative stress) (Ilhan et al., 2004, Free Radic Biol Med, 37, 386e394). This report has shown that treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. CAPE might exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of NFkB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase enzyme. A detailed review article regarding with the protective effects of CAPE on major eye diseases was released seven months ago (Akyol et al., 2014, J Ocul Pharmacol Ther, 30, 700e708). We subdivided the review with respect to various pertinent eye diseases such as cataract and PCO, corneal diseases, retina and optic nerve-related diseases, ischemia/reperfusion injury of retina, and inflammation and infection-based diseases of eye. We also drew attention to the proposed mechanisms for CAPE to diminish or block inflammation as well as ROS production inducing antioxidant defense mechanism in that article. Subsequently, two more studies were published on the effects of CAPE and/or its derivatives on experimental ocular inflammation and IL-1b-induced human corneal fibroblasts (Pittala et al., 2015, Eur J Pharmacol, 752, 78e83; Yang et al., 2014 Immunopharmacol Immunotoxicol, 36, 371e377). The stimulation of the retinal pigment epithelium causes the release of a number of chemokines including IL-8 and monocyte chemotactic protein. We also would like to draw attention to a specific point on the methodology of the Choi et al. study. Since CAPE is a very hydrophobic compound, it is soluble in organic solvents such as ethanol, dimethyl sulfoxide (DMSO), and ethyl acetate (50 mg ml 1) (Akyol et al., 2012, Cell Biochem Funct, 30, 438e443), but not directly in water or aqueous media. Accordingly, one of the control groups of rats employed in

H.K. Erdemli et al. / Experimental Eye Research 138 (2015) 124e125

the Choi et al. study should have been a vehicle control group (i.e., DMSO or DMSO plus PBS) to rule out the possible adverse or beneficial effects of the solvent itself. The reason is that it is a highly hydrophobic compound. As a result, one of control group of rats should be given DMSO (or DMSO plus PBS) to eliminate possible adverse/beneficial effects of DMSO. This methodological subtlety should have been described in Methods section of the article. DMSO is known to be responsible for the attenuation of autoimmune recurrence in non-obese diabetic animal models by inducing differentiation of regulatory T cells (Lin et al., 2015 Toxicol Appl Pharmacol, 282, 207e14) and inhibiting acute and chronic inflammations in transgenic experimental autoimmune cystitis models (Kim et al., 2011, J Biomed Biotechnol, 2011, 937061. http:// dx.doi.org/10.1155/2011/937061). In view of these facts, we suggest that some details in the design of the study reported by Choi et al. were flawed, and also failed to precisely reflect the actual clinical scenario. That said, their report does correctly underscore some of

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the effects of DMSO on the immune system, and we endorse their efforts to highlight the expanding therapeutic use of CAPE in an autoimmune disorder that affects the eye. Their findings concerning the molecular mechanism of CAPE, with regard to how it ameliorates disease symptoms, are also noteworthy and show once again that CAPE treatment limits the severity of EAU in mice by attenuating retinal migration of immune cells via ‘suppression of NFkB’. Financial support None. Conflict of interest No conflicting relationship exists for the authors.

Comment on 'Caffeic acid phenethyl ester lessens disease symptoms in an experimental autoimmune uveoretinitis mouse model' by Choi J.H. et al. [Exp. Eye Res. 134 (2015) 53-62].

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