CXCL1 but not IL-6 is required for recurrent herpetic stromal keratitis
| Autor: | Chelsea R. Del Rosso, Patrick M. Stuart, Xiao-Tang Yin, Devin M. West |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Chemokine
Neutrophils animal diseases Chemokine CXCL1 T-Lymphocytes Immunology Inflammation Herpesvirus 1 Human Receptors Interleukin-8B Article Keratitis Proinflammatory cytokine Cornea Mice medicine Immunology and Allergy Animals CXC chemokine receptors Interleukin 6 Mice Knockout biology Interleukin-6 Macrophages Antibodies Monoclonal respiratory system medicine.disease eye diseases CXCL1 Killer Cells Natural Mice Inbred C57BL medicine.anatomical_structure Neutrophil Infiltration biology.protein Keratitis Herpetic sense organs medicine.symptom |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 192(4) |
| ISSN: | 1550-6606 |
| Popis: | Herpetic stromal keratitis (HSK) is characterized by an inflammatory response that includes neutrophils, macrophages, NK cells, and T cells. The factors that are responsible for this inflammation are proinflammatory cytokines and chemokines. Many of these factors have been defined for primary disease, but relatively few have been investigated during recurrent HSK. The present study was designed to determine the role that two of these factors, IL-6 and CXCL1, play during recurrent HSK. Results clearly indicate that unlike primary disease, IL-6 plays no role in recurrent HSK. However, the presence of CXCL1 is required for recurrent HSK as evidenced by the lack of corneal disease in mice treated with anti-CXCL1 Ab. This was confirmed using mice lacking the primary receptor for CXCL1, CXCR2. Corneal disease in this strain was significantly reduced compared with wild-type C57BL/6 controls. Unexpectedly, lack of disease occurs even though CXCL1 knockout mice display increased viral shedding at the cornea. The primary mechanism that CXCL1 plays during disease is its ability to stimulate neutrophils to infiltrate the cornea following reactivation. This paper provides further evidence that primary HSK and recurrent HSK possess overlapping yet distinct disease mechanisms. |
| Databáze: | OpenAIRE |
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