The role of neutrophils in corneal wound healing in HO-2 null mice.
Our studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was underta...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3117875?pdf=render |
| _version_ | 1811209428755546112 |
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| author | Giuseppina Marrazzo Lars Bellner Adna Halilovic Giovanni Li Volti Filippo Drago Michael W Dunn Michal Laniado Schwartzman |
| author_facet | Giuseppina Marrazzo Lars Bellner Adna Halilovic Giovanni Li Volti Filippo Drago Michael W Dunn Michal Laniado Schwartzman |
| author_sort | Giuseppina Marrazzo |
| collection | DOAJ |
| description | Our studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was undertaken to examine the possible relationship between HO-2 and the recruitment of neutrophils following a corneal surface injury in wild type (WT) and HO-2 knockout (HO-2(-/-)) mice treated with Gr-1 monoclonal antibody to deplete peripheral neutrophils. Epithelial injury was performed by removing the entire corneal epithelium. Infiltration of inflammatory cell into the cornea in response to injury was higher in HO-2(-/-) than in WT. However, the rate of corneal wound closure following neutrophil depletion was markedly inhibited in both WT and HO-2(-/-) mice by 60% and 85%, respectively. Neutropenia induced HO-1 expression in WT but not in HO-2(-/-) mice. Moreover, endothelial cells lacking HO-2 expressed higher levels of the Midkine and VE-cadherin and displayed strong adhesion to neutrophils suggesting that perturbation in endothelial cell function caused by HO-2 depletion underlies the increased infiltration of neutrophils into the HO-2(-/-) cornea. Moreover, the fact that neutropenia worsened epithelial healing of the injured cornea in both WT and HO-2(-/-) mice suggest that cells other than neutrophils contribute to the exaggerated inflammation and impaired wound healing seen in the HO-2 null cornea. |
| first_indexed | 2024-04-12T04:39:13Z |
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| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-12T04:39:13Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-a0410c87e0bb427f800ef59a69c43c732022-12-22T03:47:42ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0166e2118010.1371/journal.pone.0021180The role of neutrophils in corneal wound healing in HO-2 null mice.Giuseppina MarrazzoLars BellnerAdna HalilovicGiovanni Li VoltiFilippo DragoMichael W DunnMichal Laniado SchwartzmanOur studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was undertaken to examine the possible relationship between HO-2 and the recruitment of neutrophils following a corneal surface injury in wild type (WT) and HO-2 knockout (HO-2(-/-)) mice treated with Gr-1 monoclonal antibody to deplete peripheral neutrophils. Epithelial injury was performed by removing the entire corneal epithelium. Infiltration of inflammatory cell into the cornea in response to injury was higher in HO-2(-/-) than in WT. However, the rate of corneal wound closure following neutrophil depletion was markedly inhibited in both WT and HO-2(-/-) mice by 60% and 85%, respectively. Neutropenia induced HO-1 expression in WT but not in HO-2(-/-) mice. Moreover, endothelial cells lacking HO-2 expressed higher levels of the Midkine and VE-cadherin and displayed strong adhesion to neutrophils suggesting that perturbation in endothelial cell function caused by HO-2 depletion underlies the increased infiltration of neutrophils into the HO-2(-/-) cornea. Moreover, the fact that neutropenia worsened epithelial healing of the injured cornea in both WT and HO-2(-/-) mice suggest that cells other than neutrophils contribute to the exaggerated inflammation and impaired wound healing seen in the HO-2 null cornea.http://europepmc.org/articles/PMC3117875?pdf=render |
| spellingShingle | Giuseppina Marrazzo Lars Bellner Adna Halilovic Giovanni Li Volti Filippo Drago Michael W Dunn Michal Laniado Schwartzman The role of neutrophils in corneal wound healing in HO-2 null mice. PLoS ONE |
| title | The role of neutrophils in corneal wound healing in HO-2 null mice. |
| title_full | The role of neutrophils in corneal wound healing in HO-2 null mice. |
| title_fullStr | The role of neutrophils in corneal wound healing in HO-2 null mice. |
| title_full_unstemmed | The role of neutrophils in corneal wound healing in HO-2 null mice. |
| title_short | The role of neutrophils in corneal wound healing in HO-2 null mice. |
| title_sort | role of neutrophils in corneal wound healing in ho 2 null mice |
| url | http://europepmc.org/articles/PMC3117875?pdf=render |
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