Endophthalmitis

Phillip, S.; Michelle, C.

doi:10.5772/29130

Advances in Ophthalmology 2012

DOI: 10.5772/29130

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Endophthalmitis

S. Phillip¹,

C. Michelle²

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Cited by 2 publications

(1 citation statement)

References 76 publications

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“…Endophthalmitis is an intraocular infection resulting from bacterial entry and invasion of the eye. 1 – 4 Infection stems from a variety of sources, most notably postoperative complications, ocular injuries, or endogenous sources. 1 – 7 The majority of endophthalmitis cases, however, occur following surgical procedures, such as cataract surgery, intravitreal injection, or penetrating ocular trauma.…”

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The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis

Coburn

Parrott

Miller

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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Purpose To test the hypothesis that the C-X-C chemokines CXCL1, CXCL2, and CXCL10 contribute to inflammation during Staphylococcus aureus endophthalmitis. Methods S. aureus endophthalmitis was induced by intravitreal injection of 5000 colony forming units of S. aureus into the eyes of C57BL/6J, CXCL1 −/− , CXCL2 −/− , or CXCL10 −/− mice. At 12, 24, and 36 hours postinfection, bacterial counts, intraocular inflammation, and retinal function were assessed. Based on these results, the effectiveness of intravitreal administration of anti-CXCL1 in reducing inflammation and improving retinal function was evaluated in S. aureus– infected C57BL/6J mice. Results We observed significant attenuation of inflammation and improvement in retinal function in CXCL1 −/− mice relative to C57BL/6J at 12 hours but not at 24 or 36 hours postinfection with S. aureus . Co-administration of anti-CXCL1 antibodies with S. aureus , however, did not improve retinal function or reduce inflammation at 12 hours postinfection. In CXCL2 −/− and CXCL10 −/− mice, retinal function and intraocular inflammation were not significantly different from those of C57BL/6J mice at 12 and 24 hours postinfection. At 12, 24, or 36 hours, an absence of CXCL1, CXCL2, or CXCL10 did not alter intraocular S. aureus concentrations. Conclusions CXCL1 appears to contribute to the early host innate response to S. aureus endophthalmitis, but treatment with anti-CXCL1 did not effectively limit inflammation in this infection. CXCL2 and CXCL10 did not seem to play an integral role in inflammation during the early stages of S. aureus endophthalmitis.

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mentioning

confidence: 99%

The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis

Coburn

Parrott

Miller

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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TLR4 modulates inflammatory gene targets in the retina during Bacillus cereus endophthalmitis

et al. 2018

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BackgroundEndophthalmitis is a serious intraocular infection that frequently results in significant inflammation and vision loss. Because current therapeutics are often unsuccessful in mitigating damaging inflammation during endophthalmitis, more rational targets are needed. Toll-like receptors (TLRs) recognize specific motifs on invading pathogens and initiate the innate inflammatory response. We reported that TLR4 contributes to the robust inflammation which is a hallmark of Bacillus cereus endophthalmitis. To identify novel, targetable host inflammatory factors in this disease, we performed microarray analysis to detect TLR4-dependent changes to the retinal transcriptome during B. cereus endophthalmitis.ResultsC57BL/6 J and TLR4−/− mouse eyes were infected with B. cereus and retinas were harvested at 4 h postinfection, a time representing the earliest onset of neutrophil infiltration. Genes related to acute inflammation and inflammatory cell recruitment including CXCL1 (KC), CXCL2 (MIP2-α), CXCL10 (IP-10), CCL2 (MCP1), and CCL3 (MIP1-α)) were significantly upregulated 5-fold or greater in C57BL/6 J retinas. The immune modulator IL-6, intercellular adhesion molecule ICAM1, and the inhibitor of cytokine signal transduction SOCS3 were upregulated 25-, 11-, and 10-fold, respectively, in these retinas. LIF, which is crucial for photoreceptor cell survival, was increased 6-fold. PTGS2/COX-2, which converts arachidonic acid to prostaglandin endoperoxide H2, was upregulated 9-fold. PTX3, typically produced in response to TLR engagement, was induced 15-fold. None of the aforementioned genes were upregulated in TLR4−/− retinas following B. cereus infection.ConclusionsOur results have identified a cohort of mediators driven by TLR4 that may be important in regulating pro-inflammatory and protective pathways in the retina in response to B. cereus intraocular infection. This supports the prospect that blocking the activation of TLR-based pathways might serve as alternative targets for Gram-positive and Gram-negative endophthalmitis therapies in general.Electronic supplementary materialThe online version of this article (10.1186/s12886-018-0764-8) contains supplementary material, which is available to authorized users.

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Endophthalmitis

Cited by 2 publications

References 76 publications

The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis

The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis

TLR4 modulates inflammatory gene targets in the retina during Bacillus cereus endophthalmitis

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