A Comparison of Recurrent and Primary Herpes Simplex Keratitis in NIH Inbred Mice

Miller, Judith Kelvin; Laycock, Keith A.; Umphress, J A; Hook, K K; Stuart, Patrick M.; Pepose, Jay S.

doi:10.1097/00003226-199609000-00010

Cited by 31 publications

(25 citation statements)

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“…These data led us to hypothesize that in the absence of CXCL10, there is compensatory up-regulation of CXCL9, another CXCR3 ligand (30). As B6 mice do not express CXCL11, due to a frameshift mutation (36), we did not assess expression of this CXCR3 ligand chemokine.…”

Section: Discussionmentioning

confidence: 99%

CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis

et al. 2017

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Herpetic stromal keratitis (HSK) is a disease that is typically associated with reactivation of a latent HSV-1 infection. This disease is driven, in part, by chemokines that recruit leukocytes to the cornea. Surprisingly, neutralization of CXCL10 significantly reduced disease, while B6-CXCL10−/− mice exhibited worse disease compared with similarly infected wild-type controls. We hypothesized that compensatory up-regulation of CXCL9 occurs in the absence of CXCL10. Analysis of CXCL9 expression in HSV-1-infected B6 mice and B6-CXCL10−/− mice revealed significantly more CXCL9 in B6-XCL10−/− mice. Treatment of B6 and B6-CXCL10−/− mice with neutralizing antibodies to CXCL9 reduced HSK scores in B6-CXCL10−/−, but not B6 mice. We conclude that CXCL10 production worsens HSK and that CXCL9 may compensate in CXCL10-deficient animals. These studies identify the critical role that CXCL10 plays in the pathogenesis of recurrent HSK, and that CXCL9 displays its importance when CXCL10 is absent.

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Section: Discussionmentioning

confidence: 99%

CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis

et al. 2017

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“…These procedures can have unintended consequences, only work in certain mouse strains, and reactivation tends to be inefficient and difficult to reproduce in different laboratories. Moreover, the data obtained in mouse models of recurrent HSK do not suggest a marked difference in the immunopathology compared to HSK that develops following primary infection (Miller et al, 1996). Thus, most of what we know about the immune response to HSV-1 and HSK-associated immunopathology derived from mouse primary infection models.…”

Section: Animal Models Of Infectionmentioning

confidence: 99%

Herpes keratitis

Rowe

Leger

Jeon

et al. 2013

Progress in Retinal and Eye Research

260

235

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Herpes Simplex Virus-1 (HSV-1) infects the majority of the world’s population. These infections are often asymptomatic, but ocular HSV-1 infections cause multiple pathologies with perhaps the most destructive being Herpes Stromal Keratitis (HSK). HSK lesions, which are immunoinflammatory in nature, can recur throughout life and often cause progressive corneal scaring resulting in visual impairment. Current treatment involves broad local immunosuppression with topical steroids along with antiviral coverage. Unfortunately, the immunopathologic mechanisms defined in animal models of HSK have not yet translated into improved therapy. Herein, we review the clinical epidemiology and pathology of the disease and summarize the large amount of basic research regarding the immunopathology of HSK. We examine the role of the innate and adaptive immune system in the clearance of virus and the destruction of the normal corneal architecture that is typical of HSK. Our goal is to define current knowledge of the pathogenic mechanisms and recurrent nature of HSK and identify areas that require further study.

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“…16,22,26 The presence of active clinical lesions in the second post-reactivation week has been confirmed by earlier work showing an influx of inflammatory and immune cells that also peaks at this time. 22 Likewise, disease resolution at later time points correlates well with declining cell numbers and corneal clouding.…”

Section: Discussionmentioning

confidence: 54%

“…16 Recurrent herpetic ocular disease in both humans and latently infected NIH mice is characterized clinically by transient epithelial dendritic disease, focal stromal opacification, disciform endotheliitis, and neovascularization; and histologically by corneal infiltration with macrophages, Langerhans cells, and T cells of both CD4 + and CD8 + phenotypes. 1,22,24,25 Spontaneous viral reactivation in the NIH/McKrae system is rare, and UV-B-initiated corneal HSV recrudescence allows for controlled studies of the sequence of clinical and immunologic events associated with repeated episodes of viral recurrence. With this system, we have examined the pattern of cytokine expression in a mouse model of recurrent HSK.…”

Section: Discussionmentioning

confidence: 99%

Cytokine expression in murine corneas during recurrent herpetic stromal keratitis

Keadle¹,

Usui²,

Laycock³

et al. 2001

Ocular Immunology and Inflammation

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The presence of Th2 cytokines during early stages of recurrent herpetic corneal lesions indicate the presence of a mixed Th1 and Th2 cell infiltrate, which is likely associated with a memory response to viral antigens. These data suggest that disease resolution in corneas with recurrent HSK may depend upon the balance between destructive and protective cytokines at individual sites of viral recurrence.

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A Comparison of Recurrent and Primary Herpes Simplex Keratitis in NIH Inbred Mice

Cited by 31 publications

References 0 publications

CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis

CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis

Herpes keratitis

Cytokine expression in murine corneas during recurrent herpetic stromal keratitis

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