ABSTRACT
The labeled monocytes then migrate to sites of tissue inflammation attracted by chemotactic signals. In neuroinflammatory processes, macrophages can potentially leave the site of inflammation. Inflammation during the acute phase is also accompanied by blood-brain barrier (BBB) damage, which might even precede macrophage infiltration. The state of the BBB reflects several inflammatory processes, including early interaction of leukocytes and endothelial cells, opening of tight junctions due to transcytosis, and repair mechanisms. Immunohistochemistry and iron staining of lung allografts indicated that ultrasmall superparamagnetic iron oxides (USPIO) particles were taken up by the infiltrating macrophages that accumulated at the rejection site. Later macrophage tracking into soft tissue infection by phagocytosis of USPIO particles was carried out in a similar way, as originally proposed for an EAE model and extensively discussed in the earlier sections. Histological analysis and electron microscopy of the abscess confirmed intracellular accumulation of the iron oxide particles within macrophages.
