Immunohistological study of infiltrated cells and cytokines in murine herpetic keratitis

Inoue, Tomoyuki; Inoue, Yoshitsugu; Kosaki, Ryo; Inoue, Yumiko; Nishida, Kohji; Shimomura, Yoshikazu; Tano, Yasuo; Hayashi, Kozaburo

doi:10.1034/j.1600-0420.2001.790511.x

Cited by 26 publications

(26 citation statements)

References 19 publications

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“…Leukocytes are prominent participants in the immunoinflammatory pathogenesis of viral infection in the corneal stroma. Viral infection of the cornea is followed by early, marked infiltration of PMNs into the stroma, 16 whereas other cell types, including macrophages, 17 natural killer cells, 18 and T cells, 19 infiltrate the stroma at later stages. Migration to and infiltration into tissues of various leukocytes and subsequent activation of these cells are regulated by cytokines and chemokines.…”

Section: Activation Of Nf-b By Poly(i:c) In Corneal Fibroblastsmentioning

confidence: 99%

Cytokine, Chemokine, and Adhesion Molecule Expression Mediated by MAPKs in Human Corneal Fibroblasts Exposed to Poly(I:C)

Liu¹,

Kimura

Yanai³

et al. 2008

Invest. Ophthalmol. Vis. Sci.

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Section: Activation Of Nf-b By Poly(i:c) In Corneal Fibroblastsmentioning

confidence: 99%

Cytokine, Chemokine, and Adhesion Molecule Expression Mediated by MAPKs in Human Corneal Fibroblasts Exposed to Poly(I:C)

Liu¹,

Kimura

Yanai³

et al. 2008

Invest. Ophthalmol. Vis. Sci.

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“…Being one of the first responders against invading pathogens, neutrophils are highly motile and can congregate massively at the site of infection; large numbers of neutrophils (up to 80% of infiltrated leucocytes) have been detected in the airways and the lungs during human respiratory syncytial virus (RSV) (Smith et al, 2001;Wojtasiak et al, 2010;Halfhide et al, 2011), herpes simplex virus (HSV) (Wojtasiak et al, 2010), and influenza virus infections (Everard et al, 1994;Kim et al, 2000;Inoue et al, 2001;Perrone et al, 2008). The magnitude of neutrophil infiltration depends directly on the dose (Bradley et al, 2012) and on the strain of inoculated viruses (Perrone et al, 2008;Tate et al, 2011).…”

Section: Infiltration Of Neutrophils At the Site Of Virus Infectionmentioning

confidence: 99%

Neutrophils: Neglected Players in Viral Diseases

Gabriel

Her

2013

DNA and Cell Biology

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“…However, unlike in the vaginal model, the induction of these cytokines in the cornea is independent of HVEM-mediated entry of HSV-1 (44). IL-6 and CXCL10 are neutrophil and T cell chemoattractants, respectively, known to promote ocular HSV-1 pathogenesis (19,(86)(87)(88)(89), and increased expression of these chemotactic factors may lead to heavier infiltration by myeloid and lymphoid cells in WT versus HVEM KO murine corneas (44). However, siRNA-mediated knockdown of HVEM from cultured telomereimmortalized human corneal epithelial cells decreased production of IFN-␥, MIP-1␣ (CCL3), and MIP-1␤ (CCL4) after HSV-1 challenge (90).…”

Section: Hvem Alters Host Immune Responses To Hsvmentioning

confidence: 99%

Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye

Edwards

Longnecker

2017

J Virol

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As its name suggests, the host receptor herpesvirus entry mediator (HVEM) facilitates herpes simplex virus (HSV) entry through interactions with a viral envelope glycoprotein. HVEM also bridges several signaling networks, binding ligands from both tumor necrosis factor (TNF) and immunoglobulin (Ig) superfamilies with diverse, and often opposing, outcomes. While HVEM was first identified as a viral entry receptor for HSV, it is only recently that HVEM has emerged as an important host factor in immunopathogenesis of ocular HSV type 1 (HSV-1) infection. Surprisingly, HVEM exacerbates disease development in the eye independently of entry. HVEM signaling has been shown to play a variety of roles in modulating immune responses to HSV and other pathogens, and there is increasing evidence that these effects are responsible for HVEM-mediated pathogenesis in the eye. Here, we review the dual branches of HVEM function during HSV infection: entry and immunomodulation. HVEM is broadly expressed; intersects two important immunologic signaling networks; and impacts autoimmunity, infection, and inflammation. We hope that by understanding the complex range of effects mediated by this receptor, we can offer insights applicable to a wide variety of disease states.KEYWORDS HVEM, herpes simplex virus, herpes stromal keratitis H erpes simplex virus 1 (HSV-1) infects the majority of the world's population by adulthood and is responsible for the vast majority of ocular herpesvirus infections (1-3). In humans and mice, HSV-1 establishes lifelong latency in the trigeminal ganglia (TG) (4,5). Reactivations of HSV-1 in the TG can lead to anterograde movement of the virus along the ophthalmic branch of the trigeminal nerve, resulting in recurrent infection of virtually all the superficial tissues of the eye, including the cornea, conjunctiva, and eyelid (6-8). Ocular herpesvirus infections can lead to epithelial ulceration of the cornea, uveitis, and retinitis but most commonly cause herpes stromal keratitis, or HSK (9). HSK is characterized by chronic inflammation of the corneal stroma, leading to corneal thickening, opacification, scarring, and, potentially, blindness (10, 11). While reactivation accounts for the majority of human disease, most murine studies of HSK model primary infection as mice do not efficiently or reliably reactivate from latency (6).In the primary murine model of HSK, actively replicating HSV-1 in the cornea is detectable by plaque assay for up to 5 to 6 days postinfection (dpi) (9,12). Viral replication initiates HSK, as UV-inactivated or replication-deficient mutant HSV fail to induce HSK in BALB/c mice (13). However, HSK is an inflammatory disease, brought about by host infiltrates, particularly CD4 ϩ T cells and polymorphonuclear cells (PMN), that invade the murine cornea several days after replicating virus has been cleared and that persist chronically (14)(15)(16)(17)(18). A dizzying array of cytokines, chemokines, and immune cell types have been implicated in the pathogenesis of HSK, the temporal and...

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Immunohistological study of infiltrated cells and cytokines in murine herpetic keratitis

Cited by 26 publications

References 19 publications

Cytokine, Chemokine, and Adhesion Molecule Expression Mediated by MAPKs in Human Corneal Fibroblasts Exposed to Poly(I:C)

Cytokine, Chemokine, and Adhesion Molecule Expression Mediated by MAPKs in Human Corneal Fibroblasts Exposed to Poly(I:C)

Neutrophils: Neglected Players in Viral Diseases

Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye

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