Changes in the choroid plexus, responses by intrinsic epiplexus cells and recruitment from monocytes after experimental head acceleration injury in the non-human primate

Abstract

We have examined, by scanning and transmission electron microscopy, morphological changes in the choroid plexus of the lateral ventricles of the non-human primate brain after lateral head acceleration. We demonstrate passage of plasma and blood cells either through tears in blood vessels and the choroidal epithelium, or through the cells of the choroidal epithelium, 20 min after injury, together with morphological changes in that epithelium. At 3 and 4 h small cells with a reniform nucleus accumulate in the connective tissue core of the choroid plexus. We suggest that these are monocytes. At 6 and 12 h cells can be seen in enlarged intercellular spaces within the choroidal epithelium. These cells possess surface ruffles and we suggest that they are monocytes differentiating into macrophages and epiplexus cells. Further evidence for transepithelial migration of monocytes/macrophages is obtained at 7 days. However, at 28 days all blood has been removed from the surface of the choroid plexus and epiplexus cells possess an appearance typical of that in uninjured animals. The possible sources of epiplexus cells are discussed with reference to studies of responses after brain insult and of development. We have obtained no evidence in support of emperipolesis by monocytes through the choroidal epithelium. We suggest that monocytes/macrophages migrate, via an intercellular route, to differentiate into epiplexus cells, thus providing additional numbers of epiplexus cells after head injury.

Studies of the Choroid Plexus and Its Associated Epiplexus Cells in the Lateral Ventricles of Rats Following an Exposure to a Single Non-Penetrative Blast.

“…In this connection, the choroid plexus of the third ventricle in humans appears to be damaged more frequently in frontal blows, while the plexus in the lateral ventricles is at a greater risk to lateral blows (GRCEVlC, 1982, 1983cited by MAXWELL et al, 1992. Structural changes in the Choroid plexus, including an increase in number of epiplexus cells (STURROCK, 1978;ZING, 1981ZING, , 1983, have also been reported in non-human primates after an experimental head acceleration injury (MAXWELL et al, 1992). The present study was undertaken to assess the structural damage, if any, to the choroid plexus and the cerebrospinal fluid (CSF) ventricular system following a single non-penetrative blast elicited by traditional explosives used in military exercises.…”

“…Associated with this change was the common occurrence of mononuclear cells, monocytes/lymphocytes, lodged in the intercellular spaces of the epithelial cells, suggesting their transepithelial migration. Such a phenomenon was reported in baboons after experimental head acceleration injury (MAXWELL et al, 1992). Interestingly, the transepithelial migration of mononuclear cells had never been observed in normal rodents (LING, 1979) except when they were challenged with the bacterial toxin, lipopolysaccharide (LPS) (LU et al, 1994).…”

Parallel Development of Choroid Plexus Degeneration and Meningeal Inflammation in Subarachnoid Hemorrhage – Experimental Study

“…CPs are highly vulnerable to damage in brain injuries [17], infections [24] and ischemic conditions [18]. Focal cerebral ischemia in rats subjected to 6 h of occlusion of the middle cerebral artery resulted in apoptotic cell death in the CPs [8].…”

“…CPs are innervated by sympathetic and parasympathetic nerves and deteriorated autonomic centers rely on CP pathologies [2,4,23]. CPs are highly vulnerable to damage in brain injuries [17], infections [24] and ischemic conditions [18]. CPs are involved in a variety of neurological disorders, including Alzheimer's and other neurodegenerative diseases, multiple sclerosis and other inflammatory conditions, as well as infectious, traumatic, neoplastic, and systemic diseases.…”

Serum Prolidase Activity as a Biomarker for Choroid Plexus Calcification

“…CP degeneration may result in low CSF production and hyperthermic brain injury in animals. CP is highly vulnerable to damage on head injuries, infections, and ischemic conditions (Maxwell et al 1992). Furthermore, Palha et al (2012) mentioned acute peripheral inflammation in CP.…”