An intact complement system dampens cornea inflammation during acute primary HSV-1 infection

Abstract Corneal transparency is an essential characteristic necessary for normal vision. In response to microbial infection, the integrity of the cornea can become compromised as a result of the inflammatory response and the ensuing tissue pathology including neovascularization (NV) and collagen la...

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Autores principales:	Adrian Filiberti, Grzegorz B. Gmyrek, Amanda N. Berube, Derek J. Royer, Daniel J. J. Carr
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/181959dcb960480a9c1dd4c4285e6486
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spelling	oai:doaj.org-article:181959dcb960480a9c1dd4c4285e64862021-12-02T17:16:14ZAn intact complement system dampens cornea inflammation during acute primary HSV-1 infection10.1038/s41598-021-89818-92045-2322https://doaj.org/article/181959dcb960480a9c1dd4c4285e64862021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89818-9https://doaj.org/toc/2045-2322Abstract Corneal transparency is an essential characteristic necessary for normal vision. In response to microbial infection, the integrity of the cornea can become compromised as a result of the inflammatory response and the ensuing tissue pathology including neovascularization (NV) and collagen lamellae destruction. We have previously found complement activation contributes to cornea pathology-specifically, denervation in response to HSV-1 infection. Therefore, we investigated whether the complement system also played a role in HSV-1-mediated neovascularization. Using wild type (WT) and complement component 3 deficient (C3 KO) mice infected with HSV-1, we found corneal NV was accelerated associated with an increase in inflammatory monocytes (CD11b+CCR2+CD115+/−Ly6G−Ly6Chigh), macrophages (CD11b+CCR2+CD115+Ly6G−Ly6Chigh) and a subpopulation of granulocytes/neutrophils (CD11b+CCR2−CD115+Ly6G+Ly6Clow). There were also increases in select pro-inflammatory and pro-angiogenic factors including IL-1α, matrix metalloproteinases (MMP)-2, MMP-3, MMP-8, CXCL1, CCL2, and VEGF-A that coincided with increased inflammation, neovascularization, and corneal opacity in the C3 KO mice. The difference in inflammation between WT and C3 KO mice was not driven by changes in virus titer. However, viral antigen clearance was hindered in C3 KO mouse corneas suggesting the complement system has a dynamic regulatory role within the cornea once an inflammatory cascade is initiated by HSV-1.Adrian FilibertiGrzegorz B. GmyrekAmanda N. BerubeDerek J. RoyerDaniel J. J. CarrNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Adrian Filiberti Grzegorz B. Gmyrek Amanda N. Berube Derek J. Royer Daniel J. J. Carr An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
description	Abstract Corneal transparency is an essential characteristic necessary for normal vision. In response to microbial infection, the integrity of the cornea can become compromised as a result of the inflammatory response and the ensuing tissue pathology including neovascularization (NV) and collagen lamellae destruction. We have previously found complement activation contributes to cornea pathology-specifically, denervation in response to HSV-1 infection. Therefore, we investigated whether the complement system also played a role in HSV-1-mediated neovascularization. Using wild type (WT) and complement component 3 deficient (C3 KO) mice infected with HSV-1, we found corneal NV was accelerated associated with an increase in inflammatory monocytes (CD11b+CCR2+CD115+/−Ly6G−Ly6Chigh), macrophages (CD11b+CCR2+CD115+Ly6G−Ly6Chigh) and a subpopulation of granulocytes/neutrophils (CD11b+CCR2−CD115+Ly6G+Ly6Clow). There were also increases in select pro-inflammatory and pro-angiogenic factors including IL-1α, matrix metalloproteinases (MMP)-2, MMP-3, MMP-8, CXCL1, CCL2, and VEGF-A that coincided with increased inflammation, neovascularization, and corneal opacity in the C3 KO mice. The difference in inflammation between WT and C3 KO mice was not driven by changes in virus titer. However, viral antigen clearance was hindered in C3 KO mouse corneas suggesting the complement system has a dynamic regulatory role within the cornea once an inflammatory cascade is initiated by HSV-1.
format	article
author	Adrian Filiberti Grzegorz B. Gmyrek Amanda N. Berube Derek J. Royer Daniel J. J. Carr
author_facet	Adrian Filiberti Grzegorz B. Gmyrek Amanda N. Berube Derek J. Royer Daniel J. J. Carr
author_sort	Adrian Filiberti
title	An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
title_short	An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
title_full	An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
title_fullStr	An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
title_full_unstemmed	An intact complement system dampens cornea inflammation during acute primary HSV-1 infection
title_sort	intact complement system dampens cornea inflammation during acute primary hsv-1 infection
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/181959dcb960480a9c1dd4c4285e6486
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An intact complement system dampens cornea inflammation during acute primary HSV-1 infection

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