Beschreibung:
<jats:title>Abstract</jats:title><jats:p>Cellular and humoral inflammations play important roles in ischemic brain injury. The effectiveness of immunomodulatory therapies may critically depend on the chosen experimental model. Our purpose was to compare the post‐ischemic neuroinflammation among murine permanent and transient middle cerebral artery occlusion (<jats:styled-content style="fixed-case">MCAO</jats:styled-content>) models. Permanent <jats:styled-content style="fixed-case">MCAO</jats:styled-content> was induced by transtemporal electrocoagulation and 30 minutes or 90 minutes transient <jats:styled-content style="fixed-case">MCAO</jats:styled-content> was induced by intraluminal filament in C57BL/6 mice. Infiltration of leukocyte subpopulations was quantified by immunohistochemistry and fluorescence‐activated cell sorting. Cerebral cytokine and adhesion molecule expression was measured by real‐time polymerase chain reaction (<jats:styled-content style="fixed-case">RT‐PCR</jats:styled-content>). Neutrophil infiltration was noted at 24 h after transient <jats:styled-content style="fixed-case">MCAO</jats:styled-content>, but did not further increase until 5 days in the permanent <jats:styled-content style="fixed-case">MCAO</jats:styled-content> model. Few T cells were observed in both <jats:styled-content style="fixed-case">MCAO</jats:styled-content> models at 24 h, but permanent <jats:styled-content style="fixed-case">MCAO</jats:styled-content> demonstrated much more infiltrating T cells at 5 days. Pronounced microglial activation was evident at 24 h and 5 days after permanent but not after transient <jats:styled-content style="fixed-case">MCAO</jats:styled-content>. The number of invading <jats:styled-content style="fixed-case">NK</jats:styled-content> cells and expression of <jats:styled-content style="fixed-case">MHCII</jats:styled-content> on <jats:styled-content style="fixed-case">CD11b</jats:styled-content>+ cells did not differ among the three groups. Five days after <jats:styled-content style="fixed-case">MCAO</jats:styled-content>, the expression of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐1, <jats:styled-content style="fixed-case">TNF</jats:styled-content>‐α and <jats:styled-content style="fixed-case">IFN</jats:styled-content>‐γ and of the adhesion molecules <jats:styled-content style="fixed-case">ICAM</jats:styled-content>‐1 and <jats:styled-content style="fixed-case">VCAM</jats:styled-content>‐1 was significantly higher in the permanent than in the transient <jats:styled-content style="fixed-case">MCAO</jats:styled-content> groups. Cellular and humoral inflammation differs substantially among commonly used <jats:styled-content style="fixed-case">MCAO</jats:styled-content> models. Neuroinflammation is more pronounced after permanent electrocoagulatory <jats:styled-content style="fixed-case">MCAO</jats:styled-content> compared with 30 minutes and 90 minutes filament‐<jats:styled-content style="fixed-case">MCAO</jats:styled-content>.</jats:p>