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IL-10 deficiency exacerbates the brain inflammatory response to permanent ischemia without preventing resolution of the lesion

AuthorsPérez-de-Puig, Isabel ; Miró-Mur, Francesc; Salas-Perdomo, Angélica ; Bonfill-Teixidor, Ester ; Ferrer-Ferrer, Maura; Márquez-Kisinousky, Leonardo ; Planas, Anna M.
Issue Date2013
PublisherNature Publishing Group
CitationJournal of Cerebral Blood Flow and Metabolism 33(12): 1955-1966 (2013)
AbstractStroke 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.
DescriptionEl pdf del artículo es la versión post-print.
Publisher version (URL)http://dx.doi.org/10.1038/jcbfm.2013.155
Identifiersdoi: 10.1038/jcbfm.2013.155
issn: 0271-678X
e-issn: 1559-7016
Appears in Collections:(IIBB) Artículos
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