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Title: | IL-10 deficiency exacerbates the brain inflammatory response to permanent ischemia without preventing resolution of the lesion |
Authors: | Pérez-de-Puig, Isabel ![]() ![]() ![]() ![]() ![]() |
Issue Date: | 2013 |
Publisher: | Nature Publishing Group |
Citation: | Journal of Cerebral Blood Flow and Metabolism 33(12): 1955-1966 (2013) |
Abstract: | Stroke induces inflammation that can aggravate brain damage. This work examines whether interleukin-10 (IL-10) deficiency exacerbates inflammation and worsens the outcome of permanent middle cerebral artery occlusion (pMCAO). Expression of IL-10 and IL-10 receptor (IL-10R) increased after ischemia. From day 4, reactive astrocytes showed strong IL-10R immunoreactivity. Interleukin-10 knockout (IL-10 KO) mice kept in conventional housing showed more mortality after pMCAO than the wild type (WT). This effect was associated with the presence of signs of colitis in the IL-10 KO mice, suggesting that ongoing systemic inflammation was a confounding factor. In a pathogen-free environment, IL-10 deficiency slightly increased infarct volume and neurologic deficits. Induction of proinflammatory molecules in the IL-10 KO brain was similar to that in the WT 6 hours after ischemia, but was higher at day 4, while differences decreased at day 7. Deficiency of IL-10 promoted the presence of more mature phagocytic cells in the ischemic tissue, and enhanced the expression of M2 markers and the T-cell inhibitory molecule CTLA-4. These findings agree with a role of IL-10 in attenuating local inflammatory reactions, but do not support an essential function of IL-10 in lesion resolution. Upregulation of alternative immunosuppressive molecules after brain ischemia can compensate, at least in part, the absence of IL-10. © 2013 ISCBFM. |
Description: | El pdf del artículo es la versión post-print. |
Publisher version (URL): | http://dx.doi.org/10.1038/jcbfm.2013.155 |
URI: | http://hdl.handle.net/10261/89167 |
DOI: | 10.1038/jcbfm.2013.155 |
Identifiers: | doi: 10.1038/jcbfm.2013.155 issn: 0271-678X e-issn: 1559-7016 |
Appears in Collections: | (IIBB) Artículos |
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