<i>Bacillus cereus</i>Induces Permeability of an In Vitro Blood-Retina Barrier

Moyer, Andrea; Ramadan, R.; Thurman, Joshua M.; Burroughs, Adam; Callegan, Michelle C.

doi:10.1128/iai.01330-07

Cited by 37 publications

(40 citation statements)

References 64 publications

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“…When analyzed by Western, ZO-1 expression was not detected and occludin expression was <5% by 12 h postinfection. Retinal occludin signal was lost more rapidly than ZO-1 during early infection, corroborating similar findings in RPE monolayers in vitro 13. ZO-1 and occludin were detected at 12 h postinfection via immunohistochemistry, but signals were intermittent.…”

Section: Discussionsupporting

confidence: 85%

“…Because in vitro data suggested that plcR- deficient B. cereus induced permeability of polarized RPE monolayers similarly to that of wild-type B. cereus ,13 we analyzed whether plcR- deficient B. cereus induced leakage of fibrin across the BOB during experimental B. cereus endophthalmitis. Histological analysis by trichrome staining demonstrated fibrin leakage into the anterior and poster chambers by 8 h, with similar dispersal throughout the eye by 12 h postinfection (Figure 7).…”

Section: Resultsmentioning

confidence: 99%

“…Outer BRB permeability has been demonstrated in an in vitro BRB system comprised of polarized RPE monolayers. B. cereus infection resulted in permeability of RPE monolayers and disruption and degradation of ZO-1 and occludin 13,20. Rapid BRB permeability occurred in vitro .…”

Section: Introductionmentioning

confidence: 99%

“…The majority of extracellular B. cereus toxins are produced under the control of a global regulator, plcR . However, non- plcR- regulated toxins have been found to be important in inducing RPE toxicity and blood retina barrier permeability in vitro 13 . B. cereus and its toxins induce an explosive infection that poses a significant threat to vision, causing loss of retinal function and complete destruction of retinal architecture in a murine model by 12 h postinfection 14.…”

Section: Introductionmentioning

confidence: 99%

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Bacillus cereus–Induced Permeability of the Blood–Ocular Barrier during Experimental Endophthalmitis

Moyer¹,

Ramadan

Novosad³

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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Purpose The purpose of this study was to determine to what extent blood retina barrier (BRB) permeability occurred during experimental Bacillus cereus endophthalmitis and whether tight junction alterations were involved in permeability. Methods Mice were intravitreally injected with 100 CFU B. cereus and eyes were analyzed at specific times postinfection for permeability to fibrin and albumin, quantitation of intraocular plasma constituent leakage, production of inflammatory cytokines, and alterations in tight junction protein localization and expression at the level of the RPE. Results B. cereus-induced leakage of albumin and fibrin into the aqueous and vitreous humor by 8 h postinfection. BRB permeability occurred as early as 4 h and increased 13.30-fold compared to uninfected controls by 8 h. Production of proinflammatory cytokines IL-6, MIP-1α, IL-1β, and KC increased over the course of infection. In the retina, ZO-1 disruption begins by 4 h, followed by decreasing occludin and ZO-1 expression at 4 and 8 h, respectively. Tubulin condensation and RPE65 degradation occurred by 12 h. A quorum sensing mutant B. cereus strain caused BRB permeability comparable to that of wild-type B. cereus. Both wild-type and mutant B. cereus sterile supernatants induced blood ocular barrier permeability similarly to that of wild-type infection. Conclusions These results indicate that BRB permeability occurs during the early stages of experimental B. cereus endophthalmitis, beginning as early as 4 h postinfection. Disruption of tight junctions at the level of the RPE may contribute to barrier breakdown. Quorum-sensing dependent factors may not significantly contribute to BRB permeability.

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Section: Discussionsupporting

confidence: 85%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Bacillus cereus–Induced Permeability of the Blood–Ocular Barrier during Experimental Endophthalmitis

Moyer¹,

Ramadan

Novosad³

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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“…66 Recent findings have demonstrated that RPE plays a crucial role during infection by secreting cytokines like IL-6 and controlling the blood-retinal barrier. 67 As they constitute the outer blood-retinal barrier, they may be providing the first line of defense in endogenous endophthalmitis, where the pathogens are entering the retina via the choroid. Although, the incidence of endogenous endophthalmitis is relatively low, it is very common in immune-compromised individuals like diabetics.…”

Section: Retinal Innate Immunitymentioning

confidence: 99%

Muller Glia in Retinal Innate Immunity: A Perspective on Their Roles in Endophthalmitis

et al. 2013

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Müller cells are the predominant glial cell type in the retina and have a unique anatomy, with processes that span the entire retinal thickness. Although extensive morphological and physiological studies of Müller glia have been performed, much less is known about their role in retinal innate immunity, specifically in infectious endophthalmitis. They were found to express Toll-like receptors (TLRs), a major family of pattern recognition receptors (PRRs) that mediate innate responses and provide an important mechanism by which Müller glia are able to sense both pathogen- and host-derived ligands in the vitreous and the retina. An increasing body of evidence suggests that TLR-signaling mediates beneficial effects in the retina via production of pro-inflammatory cytokines/chemokines, antimicrobial peptides and neuroprotective growth factors to restore tissue homeostasis. In this review, we discussed retinal innate immunity in general with emphasis on the role of Müller glia in initiating retinal innate defense.

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