Role of Neutrophils in Breakdown of the Blood-Retinal Barrier Following Intravitreal Injection of Platelet-activating Factor

Smith, D.C.; Lee, Eun Koo; Saloupis, Peter; Davis, Janice K.; Hatchell, Diane L.

doi:10.1006/exer.1994.1127

Cited by 11 publications

(10 citation statements)

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“…Therefore, cells sensitive to leucotoxins seem to exist within the vitreous, may be as the small number of macrophages normally present on the surface of the retina. It has been reported that platelet-activating factor may participate in the breakdown of the blood-retinal barrier [29]. Therefore, inflammatory cells sensitive to the leucotoxins remain to be characterised.…”

Section: Discussionmentioning

confidence: 99%

Channel-Forming Leucotoxins from Staphylococcus Aureus cause Severe Inflammatory Reactions in a Rabbit Eye Model

Siqueira¹,

Speeg-Schatz

Freitas

et al. 1997

Journal of Medical Microbiology

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Panton-Valentine leucocidin arises from the combination of one S component (LukS-PV) with one F component (LukF-PV), whereas y-haemolysin comprises two S components (HlgA and HlgC) with one F component HlgB. The intravitreal injection of rabbit eye with the six combinations (S + F) of channel-forming leucotoxins produced by Staphylococcus aureus ATCC 49775 induced acute inflammatory reactions depending on time and doses of toxins. These reactions involved posterior chamber as well as anterior chamber and conjunctiva, eyelids and annexes. Histological examination confirmed the involvement of eye tissues and the disruption of the retinal barrier. The lesions began only 4 h after injections and persisted for at least 5 days. Clinical and biological effects of each leucotoxin were modulated by the speed of onset and intensity of inflammation and necrosis, leading to a functional classification according to the severity of the lesions (HlgA + LukF-PV > HlgA + HlgB 3 LukS-PV + HlgB 3 LukS-PV + LukF-PV > HlgC + HlgB 3 HlgC + LukF-PV). Moreover, N-acetyl p-D glucosaminidase assays on crude extracts of vitreous revealed granules and granule secretions 'from polymorphonuclear cells with levels according the above classification. These results show that channel-forming leucotoxins have a very significant inflammatory activity. As most S. aureus strains produce two or even six leucotoxins depending on the production of Panton-Valentine leucocidin, these compounds could be considered to be virulence factors.

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Section: Discussionmentioning

confidence: 99%

Channel-Forming Leucotoxins from Staphylococcus Aureus cause Severe Inflammatory Reactions in a Rabbit Eye Model

Siqueira¹,

Speeg-Schatz

Freitas

et al. 1997

Journal of Medical Microbiology

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“…PAF interacts with P-selectins of retinal and choroidal vascular endothelium, inducing endothelial damage and vascular thrombosis [103]. The migration of leukocytes to vascular endothelium and its subsequent disruption, the activation of phospholipases and proteases, and the disturbance of permeability of mitochondrial pores are implicated in the cytotoxic effect of PAF in retinal vascular endothelial cells [104][105][106][107]. are the major anti-VEGF agents used in treatment of wet ARMD [108].…”

Section: Inflammatory Mediators and Oxidative Stressmentioning

confidence: 99%

Age-Related Macular Degeneration: Pathogenesis, Genetic Background, and the Role of Nutritional Supplements

Moschos

Nitoda

Chatziralli

et al. 2014

Journal of Chemistry

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Age-related macular degeneration (ARMD) is the leading cause of severe vision loss and blindness worldwide, mainly affecting people over 65 years old. Dry and wet ARDM are the main types of the disease, which seem to have a multifactorial background. The aim of this review is to summarize the mechanisms of ARMD pathogenesis and exhibit the role of diet and nutritional supplements in the onset and progression of the disease. Environmental factors, such as smoking, alcohol, and, diet appear to interact with mutations in nuclear and mitochondrial DNA, contributing to the pathogenesis of ARMD. Inflammatory mediators and oxidative stress, induced by the daily exposure of retina to high pressure of oxygen and light radiation, have been also associated with ARMD lesions. Other than medical and surgical therapies, nutritional supplements hold a significant role in the prevention and treatment of ARMD, eliminating the progression of macular degeneration.

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“…Activation of phospholipase A2 is the first step in the synthesis of lipid second messengers, including prostaglandins (PGs), leukotrienes, and platelet activating factor (PAF). PAF, the most active inflammatory mediator known,27 has been shown to promote vascular permeability in a number of different vascular beds27-30 including the retinal vasculature 31. PGs are thought to contribute to the pathogenesis of post-surgical and inflammatory macular oedema for several reasons.…”

Section: Soluble Factors Implicated In Brb Breakdownmentioning

confidence: 99%

“…Studies of this type in rabbits have provided insights regarding potential mediators and the mechanisms by which they compromise the BRB,19 31 37 58-60 but although rabbit retinal vessels have tight junctions and form a BRB, their limited distribution to the central retina and the relative lability of the BRB in rabbits, raise questions regarding the relevance of findings in rabbits to human disease processes. Rats and mice have holangiotic retinas that are similar to humans in most respects, except for the absence of a macula.…”

Section: Animal Models For Macular Oedemamentioning

confidence: 99%

Macular oedema: the role of soluble mediators

Kent

Vinores

Campochiaro³

2000

British Journal of Ophthalmology

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Extracellular accumulation of fluid resulting in oedema is well tolerated in most tissues of the body, but in the retina, it results in dysfunction of retinal neurons. Collection of fluid in the macula is called macular oedema and when the fovea is involved, it results in decreased visual acuity. Macular oedema occurs in a wide variety of ocular diseases and is one of the most prevalent causes of vision loss in developed countries. It is the most common cause of vision loss in patients with diabetic retinopathy 1 and in other ischaemic retinopathies such as branch and central retinal vein occlusion.2 3 Macular oedema is also a major cause of decreased vision following intraocular surgery. In the literature, the term cystoid macular oedema (CMO) is often used to describe oedema occurring after surgery, 4 because collection of fluid in the macula often results in cystic changes that are visible by ophthalmoscopy. However, cystic changes can occur with any type of macular oedema, and therefore the term post-surgical macular oedema is preferred when referring to oedema occurring after any type of intraocular procedure. Macular oedema is also a frequent complication of uveitis regardless of aetiology 5 and is commonly seen in patients with retinitis pigmentosa.6 Thus, macular oedema is a component of many diVerent types of pathological conditions and is an enormous clinical problem. Macular oedema results from breakdown of the blood-retinal barrierExtravascular accumulation of fluid in the retina is normally prevented by the blood-retinal barrier (BRB). The BRB consists of adaptations of retinal blood vessels (inner BRB) and the retinal pigmented epithelium (RPE; outer BRB) that control access of fluid and solutes to the retina. One adaptation is the presence of tight junctions between adjacent retinal vascular endothelial (RVE) cells and between adjacent RPE cells. Other adaptations include an abatement in vesicular transport in RVE cells compared with vascular endothelial cells in skin 7 8 and asymmetrical distribution of proteins that regulate vectorial transport across RPE cells.

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Role of Neutrophils in Breakdown of the Blood-Retinal Barrier Following Intravitreal Injection of Platelet-activating Factor

Cited by 11 publications

References 0 publications

Channel-Forming Leucotoxins from Staphylococcus Aureus cause Severe Inflammatory Reactions in a Rabbit Eye Model

Channel-Forming Leucotoxins from Staphylococcus Aureus cause Severe Inflammatory Reactions in a Rabbit Eye Model

Age-Related Macular Degeneration: Pathogenesis, Genetic Background, and the Role of Nutritional Supplements

Macular oedema: the role of soluble mediators

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