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Figure 1 | Critical Care

Figure 1

From: Bench-to-bedside review: Burn-induced cerebral inflammation – a neglected entity?

Figure 1

Blood–brain barrier breakdown and complement C5a receptor expression in experimental burn injury. (a) Coronal sections of rat brains obtained as a function of time after experimental burn injury. Sections were then subjected to immunohistochemical staining for albumin. In the control slide, the primary antibody was omitted (no Ab) to ensure specific staining of the albumin antibody. Brain slides from sham animals (sham) were compared with brains obtained from burned rats. Note the progressive breakdown of the blood–brain barrier from 6 to 24 hours after burn injury resulting in increased cerebral accumulation of albumin. As a large systemic molecule, albumin can only cross the blood–brain barrier when this barricade is compromised. The present data are thus indicative of increasing blood–brain barrier collapse and subsequent development of cerebral edema. Coronal brain sections were obtained from sham animals and 24 hours after burn trauma, respectively, and were immunostained for (b) the C5a receptor (C5aR) and (c) the C5a-like receptor 2 (C5L2). Sections were then counterstained with Fast Blue. Areas depicted focus on the hippocampal area of the brain. Stained cells represent microglia. While there was no difference in the expression of C5aR between sham and burn rats, C5L2 expression was significantly upregulated in brains harvested from burnt animals in comparison with sham littermates. The complement system may play an important role in the development of burn-induced neuroinflammation. Slides were analyzed by light microscopy using fourfold (4×) and 40-fold (40×) magnification.

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