IMR Press / FBL / Volume 13 / Issue 12 / DOI: 10.2741/3013

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
CCL3 protects mice from corneal pathology during recurrent HSV-1 infection
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1 Department of Ophthalmology and Visual Sciences and Molecular Microbiology and Pathogenesis, Washington University Medical School, St. Louis, MO 63110, U.S.A.
Academic Editor:Daniel Carr
Front. Biosci. (Landmark Ed) 2008, 13(12), 4407–4415; https://doi.org/10.2741/3013
Published: 1 May 2008
(This article belongs to the Special Issue Neurotropic virus infections and the host immune response)
Abstract

CCL2 and CCL3 are proinflammatory chemokines that are produced during the early stages of inflammation and are known to stimulate the migration of mononuclear cells to the site of inflammation,. Previous studies addressing the role of these chemokines during primary herpetic stromal keratitis (HSK), have suggested that CCL2 is involved in reducing corneal disease and that CCL3 is involved in promoting this disease. We addressed the role that these chemokines play in a recurrent model of HSK. Results from these studies did not demonstrate a significant role for CCL2 except for very early time points following reactivation of virus. Surprisingly, mice deficient in CCL3 did not have significantly reduced recurrent disease, , but in fact showed significantly enhanced disease. This argues that CCL3 might play an ameliorative role during recurrent HSK. In addition, we observed that these same CCL3 deficient mice showed increased resistance to viral-induced mortality following infection with HSV-1. Taken together, these results suggest that CCL3 plays a significant protective role during recurrent HSK and is involved in enhancing lethality.

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