Host defense against bacterial keratitis

O’Callaghan, Richard J.; Girgis, Dalia O.; Dajcs, Joseph J.; Sloop, Gregory D.

doi:10.1076/ocii.11.3.171.17351

Cited by 15 publications

(12 citation statements)

References 10 publications

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“…Staphylococcus aureus a-toxin is the archetype of pore-forming toxins (PFT) [1][2][3], and an important virulence factor of S. aureus [4][5][6][7][8][9][10][11][12][13][14]. It is secreted as a monomer of 34 kDa and binds to a wide variety of target cells.…”

Section: Introductionmentioning

confidence: 99%

Elimination of a bacterial pore‐forming toxin by sequential endocytosis and exocytosis

et al. 2008

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Bacterial pore forming toxin Endocytosis Exosome Innate defence mechanism Staphylococcus aureus a b s t r a c t Staphylococcus aureus a-toxin is the archetype of bacterial pore forming toxins and a key virulence factor secreted by the majority of clinical isolates of S. aureus. Toxin monomers bind to target cells and oligomerize to form small b-barrel pores in the plasma membrane. Many nucleated cells are able to repair a limited number of lesions by unknown, calcium-independent mechanisms. Here we show that cells can internalize a-toxin, that uptake is essential for cellular survival, and that pore-complexes are not proteolytically degraded, but returned to the extracellular milieu in the context of exosome-like structures, which we term toxosomes.

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Section: Introductionmentioning

confidence: 99%

Elimination of a bacterial pore‐forming toxin by sequential endocytosis and exocytosis

et al. 2008

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“…When S. aureus penetrates the corneal epithelium and the corneal stroma, there is rapid bacterial replication, production of toxins, including hemolytic ␣-toxin, and severe tissue damage, leading to corneal opacity. S. aureus infection also stimulates extensive neutrophil infiltration to the corneal stroma, and subsequent degranulation and release of cytotoxic mediators further contribute to the pathogenesis of this disease (11,13,25,26,37).…”

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confidence: 99%

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Sun¹,

Hise

Kalsow³

et al. 2006

Infect Immun

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Toll-like receptors (TLRs) expressed by the corneal epithelium represent a first line of host defense to microbial keratitis. The current study examined the role of TLR2, TLR4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD88) in a Staphylococcus aureus model of corneal inflammation. The corneal epithelia of C57BL/6, TLR2 ؊/؊ , TLR4 ؊/؊ , TLR9 ؊/؊ , and MyD88 ؊/؊ mice were abraded using a trephine and epithelial brush and were exposed to heat-or UV-inactivated S. aureus clinical strain 8325-4 and other clinical isolates. Corneal thickness and haze were measured by in vivo confocal microscopy, neutrophil recruitment to the corneal stroma was quantified by immunohistochemistry, and cytokine production was measured by enzyme-linked immunosorbent assay. The exposure of corneal epithelium to S. aureus induced neutrophil recruitment to the corneal stroma and increased corneal thickness and haze in control C57BL/6 mice but not in TLR2 ؊/؊ or MyD88 ؊/؊ mice. The responses of TLR4 ؊/؊ and TLR9 ؊/؊ mice were similar to those of C57BL/6 mice. S. aureus-induced cytokine production by corneal epithelial cells and neutrophils was also significantly reduced in TLR2 ؊/؊ mice compared with that in C57BL/6 mice. These findings indicate that S. aureus-induced corneal inflammation is mediated by TLR2 and MyD88 in resident epithelial cells and infiltrating neutrophils.

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“…[11][12][13][14][15] The onset of significant pathological effects in both models correlated with the point at which maximum growth of the bacteria was first achieved (ie, approximately 1 million bacteria per cornea). [11][12][13][14][15] One major aspect of this model that differs from the intrastromal injection model of Staphylococcus keratitis is that the infected corneal flaps became dislodged at 20 hours (Figure 1), an event that required termination of the experiment to maintain accurate bacterial quantification. Rao et al 16 and Tungsiripat et al 17 described a model of Staphylococcus keratitis initiated by infection of a corneal flap.…”

Section: Discussionmentioning

confidence: 99%

Fluoroquinolone therapy in a rabbit model of post-LASIK methicillin-resistant Staphylococcus aureus keratitis

Balzli

McCormick

Caballero

et al. 2008

Journal of Cataract and Refractive Surgery

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Host defense against bacterial keratitis

Abstract: PLA(2) is a major host-defense component of rabbit tears. Alpha-toxin is a major mediator of corneal damage, and antibody to alpha-toxin reduces pathologic changes during keratitis.

Cited by 15 publications

References 10 publications

Elimination of a bacterial pore‐forming toxin by sequential endocytosis and exocytosis

Elimination of a bacterial pore‐forming toxin by sequential endocytosis and exocytosis

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Fluoroquinolone therapy in a rabbit model of post-LASIK methicillin-resistant Staphylococcus aureus keratitis

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