ArticleJournal of virology2013
Absence of CXCL10 aggravates herpes stromal keratitis with reduced primary neutrophil influx in mice.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Role of Neutrophils on the Ocular Surface.International journal of molecular sciences · 2021Pooled it
- NF-κB/OCT-1 Mediated Upregulation of CXCL14 Chemokine Mobilizes Mucosal Effector Memory CD44+CD62L-CD4+ and CD8+ TEM Cells, and NK Cells Associated with Protection Against Genital Herpes.Pathogens & immunity · 2026Article
- Suppression of annexin A1 and its receptor reduces herpes simplex virus 1 lethality in mice.PLoS pathogens · 2022Article
- Initial TK-deficient HSV-1 infection in the lip alters contralateral lip challenge immune dynamics.Scientific reports · 2022Article
- Absence of the lectin-like domain of thrombomodulin reduces HSV-1 lethality of mice with increased microglia responses.Journal of neuroinflammation · 2022Article
- Cytokines and chemokines: The vital role they play in herpes simplex virus mucosal immunology.Frontiers in immunology · 2022Review
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Microglia Reduce Herpes Simplex Virus 1 Lethality of Mice with Decreased T Cell and Interferon Responses in Brains.International journal of molecular sciences · 2021Article
- C-X-C Chemokines Influence Intraocular Inflammation During Bacillus Endophthalmitis.Investigative ophthalmology & visual science · 2021Article
- Pathogenesis of Herpes Stromal Keratitis: Immune Inflammatory Response Mediated by Inflammatory Regulators.Frontiers in immunology · 2020Review
- Ocular Glands Become Infected Secondarily to Infectious Keratitis and Play a Role in Corneal Resistance to Infection.Journal of virology · 2019Article
- Pathogenesis of herpes simplex keratitis: The host cell response and ocular surface sequelae to infection and inflammation.The ocular surface · 2019Review
- CXCL10 suppression of hem- and lymph-angiogenesis in inflamed corneas through MMP13.Angiogenesis · 2017Article
- Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment.Neurology(R) neuroimmunology & neuroinflammation · 2017Article
- CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis.Virology · 2017Article
- Thymidine Kinase-Negative Herpes Simplex Virus 1 Can Efficiently Establish Persistent Infection in Neural Tissues of Nude Mice.Journal of virology · 2017Article
- Article
- Diversity of heparan sulfate and HSV entry: basic understanding and treatment strategies.Molecules (Basel, Switzerland) · 2015Review
- Hypersensitivity Responses in the Central Nervous System.Frontiers in immunology · 2015Review
- Tranylcypromine reduces herpes simplex virus 1 infection in mice.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) replication initiates inflammation and angiogenesis responses in the cornea to result in herpetic stromal keratitis (HSK), which is a leading cause of infection-induced vision impairment. Chemokines are secreted to modulate HSK by recruiting leukocytes, which affect virus growth, and by influencing angiogenesis. The present study used a murine infection model to investigate the significance of the chemokine CXC chemokine ligand 10 (CXCL10; gamma interferon-inducible protein 10 [IP-10]) in HSK. Here, we show that HSV-1 infection of the cornea induced CXCL10 protein expression in epithelial cells. The corneas of mice with a targeted disruption of the gene encoding CXCL10 displayed decreases in levels of neutrophil-attracting cytokine (interleukin-6), primary neutrophil influx, and viral clearance 2 or 3 days postinfection. Subsequently, absence of CXCL10 aggravated HSK with elevated levels of interleukin-6, chemokines for CD4(+) T cells and/or neutrophils (macrophage inflammatory protein-1α and macrophage inflammatory protein-2), angiogenic factor (vascular endothelial growth factor A), and secondary neutrophil influx, as well as infiltration of CD4(+) T cells to exacerbate opacity and angiogenesis in the cornea at 14 and up to 28 days postinfection. Our results collectively show that endogenous CXCL10 contributes to recruit the primary neutrophil influx and to affect the expression of cytokines, chemokines, and angiogenic factors as well as to reduce the viral titer and HSK severity.
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Registered trials
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