ArticleInvestigative ophthalmology & visual science2017
ISG15 in Host Defense Against Candida albicans Infection in a Mouse Model of Fungal Keratitis.
Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- Article
- Defining the early stages of intestinal colonisation by whipworms.Nature communications · 2022Article
- GLUT3 as an Intersection of Glycerophospholipid Metabolism and the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021Article
- Immunogenetics of the Ocular Anterior Segment: Lessons from Inherited Disorders.Journal of ophthalmology · 2021Review
- ISG15 Connects Autophagy and IFN-γ-Dependent Control of Toxoplasma gondii Infection in Human Cells.mBio · 2020Article
- Review
- ISG15 Acts as a Mediator of Innate Immune Response to Pseudomonas aeruginosa Infection in C57BL/6J Mouse Corneas.Investigative ophthalmology & visual science · 2020Article
- Interferon-stimulated gene 15 (ISG15) restricts Zika virus replication in primary human corneal epithelial cells.The ocular surface · 2019Article
- ISG15 in antiviral immunity and beyond.Nature reviews. Microbiology · 2018Review
- Deregulated MicroRNA-21 Expression in Monocytes from HIV-Infected Patients Contributes to Elevated IP-10 Secretion in HIV Infection.Frontiers in immunology · 2017Article
- Emerging treatments in fungal keratitis.Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological SocietyArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Purpose: ISG15, a di-ubiquitin-like protein, is critical for controlling certain viral and bacterial infections. We sought to determine if ISG15 plays a role in corneal innate immunity against Candida albicans (C. albicans) using a C57BL/6 (B6) mouse model of human fungal keratitis. Methods: Scarified corneas of adult B6 mice were pretreated with TLR5 ligand flagellin and then inoculated with C. albicans. The expression of ISG15 and other genes involved in ISG15 conjugation (ISGylation) was determined by real-time PCR. ISG15 expression and distribution in infected corneas were assessed by immunohistochemistry. ISGylation was examined by Western blotting. siRNA knockdown and recombinant ISG15 were used to elucidate the effects of ISG15 on controlling fungal keratitis by clinical scoring, fungal number plate counting, ELISA cytokine determination, and polymorphonuclear leukocytes (PMN) infiltration measurement. Results: Heat-killed C. albicans induced expression of ISG15, and hBD2 was markedly enhanced by flagellin-pretreatment in cultured human primary corneal epithelial cells (CECs). In vivo, C. albicans infection induced the expression of ISG15, ISGylation-associated genes (UBE1L, UBCH8, and HERC5), and ISGylation in mouse CECs, all of which were enhanced by flagellin-pretreatment. siRNA knockdown of ISG15 increased keratitis severity, dampened flagellin-induced protection, and greatly suppressed the expressions of ISGylation enzymes, IFN-γ, but not CXCL2 in B6 mouse CECs. Recombinant ISG15, on the other hand, enhanced corneal innate immunity against C. albicans and suppressed infection-induced IL-1β, but not IL-Ra expression. ISG15 alone induced the expression of IL-1Ra, CXCL10, and CRAMP in mouse CECs. ISG15 was upregulated and secreted in cultured human CECs in response to challenge in a type 1 IFN-dependent manner. Conclusions: Our data, for the first time, demonstrate that ISG15 acts as an immunomodulator in the cornea and plays a critical role in controlling fungal keratitis.
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Registered trials
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