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Role of the Fas pathway in Pseudomonas aeruginosa keratitis. Invest Ophthalmol Vis Sci
, 2010
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Toll-like receptor 2 ligand-induced protection against bacterial endophthalmitis
- Journal of Infectious Diseases
, 2010
"... Background. Activation of innate immunity plays a key role in determining the outcome of an infection. Here, we investigated whether Toll-like receptors (TLRs) are involved in retinal innate response and explored the pro-phylactic use of TLR2 ligand in preventing bacterial endophthalmitis. Methods. ..."
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Background. Activation of innate immunity plays a key role in determining the outcome of an infection. Here, we investigated whether Toll-like receptors (TLRs) are involved in retinal innate response and explored the pro-phylactic use of TLR2 ligand in preventing bacterial endophthalmitis. Methods. C57BL/6 mice were given intravitreal injections of Pam3Cys, a synthetic ligand of TLR2, or vehicle (phosphate-buffered saline) 24 h prior to Staphylococcus aureus inoculation. The severity of endophthalmitis was graded by slit lamp, electroretinography, histological examinations, and determination of bacterial load in the retina. The expression of cytokines/chemokines and cathelicidin-related antimicrobial peptide was assessed by enzyme-linked immunosorbent assay and Western blot, respectively. Results. Intravitreal injections of Pam3Cys up-regulated TLR2 expression in the retina of C57BL/6 mice, and Pam3Cys pretreatment significantly improved the outcome of S. aureus endophthalmitis, preserved retinal structural integrity, and maintained visual function as assessed by electroretinography in C57BL/6 mice. Furthermore, Pam3Cys pretreatment activated retinal microglia cells, induced the expression of cathelicidin-related antimicrobial peptide, and remarkably reduced the bacterial load. Conclusions. This is the first report that highlights the existence and role of TLR2 in retinal innate immune response to S. aureus infection and suggests that modulation of TLR activation provides a novel prophylactic
Authors
, 2008
"... See next page for additional authors This item is available as part of Virtual Commons, the open-access institutional repository of Bridgewater State University, Bridgewater, Massachusetts. Virtual Commons Citation ..."
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See next page for additional authors This item is available as part of Virtual Commons, the open-access institutional repository of Bridgewater State University, Bridgewater, Massachusetts. Virtual Commons Citation
A Role for Tumor Necrosis Factor-␣ in Experimental Bacillus cereus Endophthalmitis Pathogenesis
, 2008
"... PURPOSE. To determine the contribution of tumor necrosis factor-alpha (TNF␣) in the pathogenesis of experimental Bacillus cereus endophthalmitis. METHODS. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNF␣ knockout mice (TNF␣ Ϫ/Ϫ , B6. ..."
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PURPOSE. To determine the contribution of tumor necrosis factor-alpha (TNF␣) in the pathogenesis of experimental Bacillus cereus endophthalmitis. METHODS. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNF␣ knockout mice (TNF␣ Ϫ/Ϫ , B6.129S6-Tnf tm1Gk1 /J). At various times after infection, eyes were analyzed by electroretinography and were harvested for quantitation of bacteria, myeloperoxidase, proinflammatory cytokines and chemokines, and histologic analysis. RESULTS. B. cereus replicated more rapidly in the eyes of TNF␣ Ϫ/Ϫ mice than in the eyes of B6.129F1 mice. Retinal function decreased more rapidly in TNF␣ Ϫ/Ϫ mice than in B6.129F1 mice. Retinal layers were not as structurally intact at 6 and 12 hours after infection in TNF␣ Ϫ/Ϫ eyes as in B6.129F1 eyes. Histologic analysis suggested less polymorphonuclear leukocyte (PMN) infiltration into the vitreous of TNF␣ Ϫ/Ϫ mice than of B6.129F1 mice. B6.129F1 eyes also had greater myeloperoxidase concentrations than did eyes of TNF␣ Ϫ/Ϫ mice. In general, concentrations of proinflammatory cytokines and chemokines (IL-1, KC, IL-6, and MIP-1␣) were greater in eyes of TNF␣ Ϫ/Ϫ mice than of B6.129F1 mice. CONCLUSIONS. TNF␣ is important to intraocular pathogen containment by PMNs during experimental B. cereus endophthalmitis. In the absence of TNF␣, fewer PMNs migrated into the eye, facilitating faster bacterial replication and retinal function loss. Although greater concentrations of proinflammatory cytokines were synthesized in the absence of TNF␣, the resultant inflammation was diminished, and an equally devastating course of infection occurred. (Invest Ophthalmol Vis Sci.
From the 1 Oklahoma Center for Neuroscience and the Departments
"... PURPOSE. To determine the contribution of tumor necrosis factor-alpha (TNF�) in the pathogenesis of experimental Bacillus cereus endophthalmitis. METHODS. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNF � knockout mice (TNF � �/ � , B ..."
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PURPOSE. To determine the contribution of tumor necrosis factor-alpha (TNF�) in the pathogenesis of experimental Bacillus cereus endophthalmitis. METHODS. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNF � knockout mice (TNF � �/ � , B6.129S6-Tnf tm1Gk1 /J). At various times after infection, eyes were analyzed by electroretinography and were harvested for quantitation of bacteria, myeloperoxidase, proinflammatory cytokines and chemokines, and histologic analysis. RESULTS. B. cereus replicated more rapidly in the eyes of TNF � �/ � mice than in the eyes of B6.129F1 mice. Retinal function decreased more rapidly in TNF � �/ � mice than in B6.129F1 mice. Retinal layers were not as structurally intact at 6 and 12 hours after infection in TNF � �/ � eyes as in B6.129F1
The SAG1 Toxoplasma gondii Surface Protein Is Not Required for Acute Ocular Toxoplasmosis in Mice �
, 2007
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RESEARCH ARTICLE Role of Staphylococcus aureus Virulence Factors in Inducing Inflammation and Vascular Permeability in a Mouse Model of Bacterial Endophthalmitis
"... Staphylococcus (S.) aureus is a common causative agent of bacterial endophthalmitis, a vision threatening complication of eye surgeries. The relative contribution of S. aureusviru-lence factors in the pathogenesis of endophthalmitis remains unclear. Here, we comprehen-sively analyzed the development ..."
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Staphylococcus (S.) aureus is a common causative agent of bacterial endophthalmitis, a vision threatening complication of eye surgeries. The relative contribution of S. aureusviru-lence factors in the pathogenesis of endophthalmitis remains unclear. Here, we comprehen-sively analyzed the development of intraocular inflammation, vascular permeability, and the loss of retinal function in C57BL/6 mouse eyes, challenged with live S. aureus, heat-killed S. aureus(HKSA), peptidoglycan (PGN), lipoteichoic acid (LTA), staphylococcal protein A (SPA), α-toxin, and Toxic-shock syndrome toxin 1 (TSST1). Our data showed a dose-dependent (range 0.01 μg/eye to 1.0 μg/eye) increase in the levels of inflammatory media-tors by all virulence factors. The cell wall components, particularly PGN and LTA, seem to induce higher levels of TNF-α, IL-6, KC, and MIP2, whereas the toxins induced IL-1β. Simi-larly, among the virulence factors, PGN induced higher PMN infiltration. The vascular per-meability assay revealed significant leakage in eyes challenged with live SA (12-fold) and HKSA (7.3-fold), in comparison to other virulence factors (~2-fold) and controls. These changes coincided with retinal tissue damage, as evidenced by histological analysis. The electroretinogram (ERG) analysis revealed a significant decline in retinal function in eyes inoculated with live SA, followed by HKSA, SPA, and α-toxin. Together, these findings dem-onstrate the differential innate responses of the retina to S. aureus virulence factors, which contribute to intraocular inflammation and retinal function loss in endophthalmitis.
doi:10.1155/2012/196094 Review Article Role of Inflammation in Endophthalmitis
"... Copyright © 2012 J. L. Vallejo-Garcia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Inflammation originating from infection ..."
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Copyright © 2012 J. L. Vallejo-Garcia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Inflammation originating from infection of the vitreous cavity is called endophthalmitis. Attention has been focused on the epidemiologic, microbiologic reports, and treatment options; unfortunately, the role of the host immune reaction in the visual function damage is still not well understood. Endophthalmitis occurs most frequently after cataract surgery. In this paper we review the published literature regarding inflammatory mediators and apoptosis during the course of endophthalmitis. Toll-like receptors, cytokines, high-mobility group box 1 proteins, aB-crystallin and apoptosis have been studied during clinical and experimental cases of endophthalmitis. Further understanding of the host-immune reaction to vitreous infection is essential for the development of new therapies. The use of intravitreal antibiotics and corticosteroids, vitrectomy and systemic antibiotics for the preservation of visual function is still discouraging. 1. Role of Inflammation in Endophthalmitis Endophtalmitis is defined as inflammation originating from infection of the vitreous cavity. The specific features of the cellular damage that is created from the excessive immune
