Mechanisms of Intraocular Inflammation

Magone, M. Teresa; Whitcup, Scott M.

doi:10.1159/000058742

Cited by 22 publications

(13 citation statements)

References 165 publications

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“…27 Inflammatory cell aggregations as detected in the present study may consist of several cell populations including activated microglial cells, T cells, macrophages and their derivates, and MGCs, 25,26 all of which may be MHC class II ϩ . The uveal inflammatory reaction in the present material was severe compared with previous results from vaccinated and nonvaccinated fish studied in our laboratory.…”

Section: Discussionmentioning

confidence: 53%

Granulomatous Uveitis Associated with Vaccination in the Atlantic Salmon

et al. 2004

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Abstract. This study addressed histologic and immunopathologic changes in ocular tissues and investigated the distribution of major histocompatibility class II (MHC class II)-positive cells in Atlantic salmon (Salmo salar) suffering from severe postvaccination disease. Twenty-nine fish with generalized inflammation, probably a result of vaccination, were investigated. One individual that had escaped vaccination was included in the study. Material was investigated by cultivation methods for fungi and bacteria. Histology using conventional staining procedures and immunohistochemistry with antisera against MHC class II ␤ chain were performed. No growth was observed from the cultivation investigations. Histology revealed occlusion of the lumen in the larger choroid vessels and in the choriocapillaris, inflammatory infiltrations and loss of structure in the choroid rete, and, in some cases, aggregations of multinucleated giant cells (MGC) and Splendore-Hoeppli material. Immunohistochemistry demonstrated massive MHC class II ϩ cellular infiltrations in the uveal tract. Such infiltrations were also seen in the ventral ciliary cleft, a condition that is associated with glaucoma. Immunoreactive cells included dendritelike cells, epithelioid cells, and MGCs. The endothelia of smaller vessels were frequently MHC class II ϩ , and immunoreactive infiltrations were seen in the optic nerve in several individuals. No pathologic changes were detected in the unvaccinated individual. In conclusion, generalized inflammatory reactions in fish may lead to severe ocular inflammation, occlusion of uveal vessels, and perivascular changes with MHC class II ϩ upregulation in cells in the uveal tract and optic nerve.

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Section: Discussionmentioning

confidence: 53%

Granulomatous Uveitis Associated with Vaccination in the Atlantic Salmon

et al. 2004

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“…Breakdown of this barrier is associated with almost every retinal disease (17,37), and infection has specifically been identified as a cause of barrier disruption (18,45). In human cases of endophthalmitis, significant localization of serum albumin in the BRB has been reported (64).…”

Section: Discussionmentioning

confidence: 99%

“…The breakdown of blood ocular barriers can lead to upregulation of adhesion molecules, leukocyte infiltration (19,27,30,38,40,67), and release of inflammatory mediators, which intensify and maintain inflammation (32,37,60). BRB permeability occurs during inflammation in an experimental autoimmune uveoretinitis model where leukocytes play an active role in permeability and tight junction disruption (68).…”

mentioning

confidence: 99%

Bacillus cereusInduces Permeability of an In Vitro Blood-Retina Barrier

Moyer¹,

Ramadan

Thurman³

et al. 2008

Infect Immun

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Most Bacillus cereus toxin production is controlled by the quorum-sensing-dependent, pleiotropic global regulator plcR, which contributes to the organism's virulence in the eye. The purpose of this study was to analyze the effects of B. cereus infection and plcR-regulated toxins on the barrier function of retinal pigment epithelium (RPE) cells, the primary cells of the blood-retina barrier. Human ARPE-19 cells were apically inoculated with wild-type or quorum-sensing-deficient B. cereus, and cytotoxicity was analyzed. plcR-regulated toxins were not required for B. cereus-induced RPE cytotoxicity, but these toxins did increase the rate of cell death, primarily by necrosis. B. cereus infection of polarized RPE cell monolayers resulted in increased barrier permeability, independent of plcR-regulated toxins. Loss of both occludin and ZO-1 expression occurred by 8 h postinfection, but alterations in tight junctions appeared to precede cytotoxicity. Of the several proinflammatory cytokines analyzed, only interleukin-6 was produced in response to B. cereus infection. These results demonstrate the deleterious effects of B. cereus infection on RPE barrier function and suggest that plcRregulated toxins may not contribute significantly to RPE barrier permeability during infection.

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“…The local levels of total IgG were considerably higher in the Brazilian than in the Swiss group. This finding indicates that either the mechanisms responsible for maintaining uveovascular barrier integrity or the time elapsing between the onset and detection of the inflammatory response differed in each population (Garweg et al, 2000;Magone and Whitcup, 1999;Vallochi et al, 2002). Evidence for the first tenet is afforded by the existence of a correlation between the levels of total IgG in paired samples of aqueous humor and serum derived from Brazilian patients but the absence of one in the Swiss group (Fig.…”

Section: Article In Pressmentioning

confidence: 98%