Cyclooxygenase (COX)-Inhibiting Drug Reduces HSV-1 Reactivation in the Mouse Eye Model

Higaki, Shiro; Watanabe, Keizo; Itahashi, Motoki; Shimomura, Yoshikazu

doi:10.1080/02713680802650377

Cited by 17 publications

(14 citation statements)

References 33 publications

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“…Gebhardt et al [56] reported that after hyperthermic stress, latently infected mice treated with celecoxib had less infectious virus on their ocular surfaces than controls (see Table 4). Higaki et al [58] reported that bromfenac sodium eye drops significantly reduced HSV-1 ocular shedding in mice induced by immunosuppression and hyperthermia. They concluded that bromfenac sodium eye drops could be a potent medication for suppressing HSV-1 reactivation [58].…”

Section: Mice and Hsv-1 Latencymentioning

confidence: 99%

Rabbit and Mouse Models of HSV-1 Latency, Reactivation, and Recurrent Eye Diseases

Webre

Hill

Nolan

et al. 2012

Journal of Biomedicine and Biotechnology

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The exact mechanisms of HSV-1 establishment, maintenance, latency, reactivation, and also the courses of recurrent ocular infections remain a mystery. Comprehensive understanding of the HSV-1 disease process could lead to prevention of HSV-1 acute infection, reactivation, and more effective treatments of recurrent ocular disease. Animal models have been used for over sixty years to investigate our concepts and hypotheses of HSV-1 diseases. In this paper we present descriptions and examples of rabbit and mouse eye models of HSV-1 latency, reactivation, and recurrent diseases. We summarize studies in animal models of spontaneous and induced HSV-1 reactivation and recurrent disease. Numerous stimuli that induce reactivation in mice and rabbits are described, as well as factors that inhibit viral reactivation from latency. The key features, advantages, and disadvantages of the mouse and rabbit models in relation to the study of ocular HSV-1 are discussed. This paper is pertinent but not intended to be all inclusive. We will give examples of key papers that have reported novel discoveries related to the review topics.

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Section: Mice and Hsv-1 Latencymentioning

confidence: 99%

Rabbit and Mouse Models of HSV-1 Latency, Reactivation, and Recurrent Eye Diseases

Webre

Hill

Nolan

et al. 2012

Journal of Biomedicine and Biotechnology

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“…20 Regarding the therapeutic effect of bromfenac eye drops in animal models, it has been shown that they reduce retinal edema triggered by lipopolysaccharide systemic injection in iovs.arvojournals.org j ISSN: 1552-5783 rats and rabbits 9,17 and prevent reactivation of herpes virus 1 in infected mice. 21 Inflammation and edema are, as well, common responses to tissue damage or disease, as has been shown for the retina in animal models of glaucoma or optic nerve injury. [22][23][24][25][26][27][28] Macroglial retinal cells, astrocytes, and Müller cells readily respond to intravitreral injections, 29 injury, or disease.…”

mentioning

confidence: 99%

Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush

Rovere

Nadal-Nicolás

Sobrado‐Calvo

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Citation: Rovere G, Nadal-Nicolás FM, Sobrado-Calvo P, et al. Topical treatment with bromfenac reduces retinal gliosis and inflammation after optic nerve crush. Invest Ophthalmol Vis Sci. 2016;57:6098-6106. DOI: 10.1167/iovs.16-20425 PURPOSE. To study the effect of topical administration of bromfenac, a nonsteroidal antiinflammatory drug (NSAID), on retinal gliosis and levels of prostaglandin E 2 (PGE 2 ) after complete optic nerve crush (ONC).METHODS. Adult albino rats were divided into the following groups (n ¼ 8 retinas/group): (1) intact, (2) intact and bromfenac treatment (twice a day during 7 days), (3) ONC (7 days), and (4) ONC (7 days) þ bromfenac treatment (twice a day during 7 days). Animals from groups 3 and 4 were imaged in vivo with spectral-domain optical coherence tomography (SD-OCT) before the procedure and 15 minutes, 3, 5, or 7 days later. Retinas from all groups were analyzed by immunodetection, Western blotting, or enzyme-linked immunoabsorbent assay (ELISA).RESULTS. Quantification of Brn3a (brain-specific homeobox/POU domain protein 3A)þ RGCs (retinal ganglion cells) in cross sections showed that bromfenac treatment does not accelerate ONC-induced degeneration. Cellular retinaldehyde binding protein 1 regulation indicated that bromfenac improves retinal homeostasis in injured retinas. Spectral-domain OCT showed that the thickness of the retina and the retinal nerve fiber layer at 7 days post ONC was significantly reduced in bromfenac-treated animals when compared to untreated animals. In agreement with these data, hypertrophy of astrocytes and Müller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment. While no changes in cyclooxygenase (COX) enzyme COX1 and COX2 expression were observed, there was a significant increase of PGE 2 after ONC that was controlled by bromfenac treatment.CONCLUSIONS. Topical administration of bromfenac is an efficient and noninvasive treatment to control the retinal gliosis and release of proinflammatory mediators that follow a massive insult to the RGC population.

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“…10 Although none of the three drug-treated groups showed any signifi cant differences from the saline solution group (P > 0.05, Welch's t test), the average copy number of viral DNA in the trigeminal ganglia of the mice treated with either etodolac or bromfenac Na eye drops was about one-tenth that of the mice treated with saline solution. However, the pranoprofen eye drops demonstrated an outcome inferior by an order of magnitude to that of the bromfenac Na eye drops in TGs.…”

Section: Resultsmentioning

confidence: 94%

“…Table 1 shows the eye swab results for the etodolac, bromfenac Na, and pranoprofen groups. 10 When the stimulation for reactivation was performed, ten of 24 eyes (41.7%) of the bromfenac Na group, fi ve of ten eyes (50.0%) of the etodolac group, and 17 of 25 eyes (68%) of the pranoprofen group showed positive results. However, compared with the results for the saline solution group (16 of 22 eyes, 72.7%), only the bromfenac Na group was signifi cantly different (P = 0.033, Fisher's exact probability test).…”

Section: Methodsmentioning

confidence: 95%

“…In our current study, 10,11 seven medications were investigated for their effi cacy in suppressing HSV-1 reactivation. These medications were oral etodolac, bromfenac sodium (Na) eye drops, pranoprofen eye drops, oral ascorbic acid, 12 oral zinc, 13 intramuscular adenosine monophosphate (AMP), 14 and intraperitoneal geldanamycin.…”

Section: Suppressing Hsv-1 Reactivationmentioning

confidence: 99%

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Suppression of herpes simplex virus 1 reactivation in a mouse eye model by cyclooxygenase inhibitor, heat shock protein inhibitor, and adenosine monophosphate

2010

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It is accepted that herpes simplex virus type 1 (HSV-1) latency occurs in the trigeminal ganglion. However, our group 1,2 and several other groups have demonstrated latent virus presence in the cornea. Negative homogenate and positive coculture provide proof of latent infection. Conventional coculture tests demonstrated HSV-1 latency in ten of the 20 eyes (50%) with herpetic stromal keratitis in the quiescent phase we examined. 1 In addition, although conventional coculture detected 50% presence, polymerase chain reaction (PCR) demonstrated HSV-1 latency in the corneas of 80% of these cases. 1 Various methods have been tried to suppress HSV-1 reactivation. Studies have shown that acyclovir, 3 propranolol, 4 thymidine kinase inhibitor, 5 helicase-primase inhibitor, 6 bupropion, 7 and oral cyclooxygenase (COX) inhibitor 8,9 effectively lower HSV-1 recurrence rates. However, the improvements registered did not prove suffi cient. Suppressing HSV-1 ReactivationIn our current study, 10,11 seven medications were investigated for their effi cacy in suppressing HSV-1 reactivation. These medications were oral etodolac, bromfenac sodium (Na) eye drops, pranoprofen eye drops, oral ascorbic acid, 12 oral zinc, 13 intramuscular adenosine monophosphate (AMP), 14 and intraperitoneal geldanamycin. 15 Etodolac, bromfenac Na eye drops, and pranoprofen are COX inhibitors. Oral etodolac is dominant in COX-2 inhibition, bromfenac Na eye drops, too, are dominant in COX-2 inhibition, 16 whereas pranoprofen eye drops are not COX-2-specifi c. 17 Ascorbic acid is vitamin C, and geldanamycin is a heat shock protein inhibitor. MethodsMice corneas were inoculated with 2.5 × 10 4 plaque forming units (PFU) of HSV-1 strain McKrae. Four weeks later, mice confi rmed to have latent HSV-1 were treated with one of the following: oral etodolac (Hypen, Nihonshinyaku, Tokyo, Japan), bromfenac Na eye drops (Bronuck, Senjyu, Tokyo, Japan), pranoprofen eye drops (Proranon, Santen, Tokyo, Japan), oral ascorbic acid (Sigma, St Louis, MO, USA), oral zinc (Sigma), intramuscular AMP (Nacalai Tesque, Kyoto, Japan), and intraperitoneal geldanamycin (InvivoGen, San Diego, CA, USA) for 4 days. As controls, saline solution eye drops (saline solution injection, Otsuka Pharmaceutical, Tokushima, Japan), oral saline solution, intramuscular saline solution, and intraperitoneal dimethyl sulfoxide (DMSO, Wako, Osaka, Japan) were used. These treatments continued from postinfection (PI) day 31 to 34 (PI day 25 to 29 in the ascorbic acid, zinc, AMP, and geldanamycin groups). The mice were given an intravenous injection of cyclophosphamide on PI day 32 (PI day 28 in the ascorbic acid, zinc, AMP, and geldanamycin groups) Jpn

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Cyclooxygenase (COX)-Inhibiting Drug Reduces HSV-1 Reactivation in the Mouse Eye Model

Abstract: Bromfenac Na eye drops can suppress HSV-1 reactivation.

Cited by 17 publications

References 33 publications

Rabbit and Mouse Models of HSV-1 Latency, Reactivation, and Recurrent Eye Diseases

Rabbit and Mouse Models of HSV-1 Latency, Reactivation, and Recurrent Eye Diseases

Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush

Suppression of herpes simplex virus 1 reactivation in a mouse eye model by cyclooxygenase inhibitor, heat shock protein inhibitor, and adenosine monophosphate

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