Ultrastructural and histophysiological studies on the blood-nerve barrier and perineurial barrier in leprosy neuropathy
- 1 January 1984
- journal article
- research article
- Published by Springer Nature in Acta Neuropathologica
- Vol. 64 (4) , 282-296
- https://doi.org/10.1007/bf00690394
Abstract
Onset and nature of ultrastructural changes in endoneurial vasa nervorum during the pathogenesis of leprosy neuropathy and possibly associated alterations in the “blood-nerve barrier” were investigated, together with perineurial barrier functioning, in mice infected 20–28 months previously withMycobacterium leprae and in (ageing) non-infected mice. Barriers were tested by i.v. administration of markers (Trypan blue and ferritin) 1–4 days before killing the mice. Twenty-eight months after infection, histopathology of sciatic nerves was comparable to that seen in sensory nerves in clinically early human (borderline-) lepromatous leprosy. Schwann cells and endoneurial macrophages were bacillated, endothelia of endoneurial vessels not, and the perineurium rarely. Many infected mice and all (ageing) controls possessed ultrastructurally and functionally normal endoneurial vessels. Their continuous endothelium with close junctions had prevented marker passage, even when surrounding endoneurial tissue cells were quite heavily bacillated. The perineurium was also normal. By contrast, in infected mice showing hind limb paralysis serious histopathologic involvement and large globi of bacilli intrafascicularly in sciatic nerves, endoneurial blood vessels were abnormal. Open endothelial junctions, extreme attenuation, fenestrations, and luminal protrusions were all features comparable to neural microangiopathy encountered in leprosy patients (Boddingius 1977a, b). The “blood-nerve barrier” clearly had become defective allowing excessive exudation of Trypan blue and ferritin, via four pathways from the vessel lumen, deep into surrounding endoneurial tissues but halted by a normal perineurial barrier. Markers in such “blue” nerves were not found in bacillated or non-bacillated Schwann cells, thus denying significant phagocytotic and lysosomal activities of Schwann cells at this stage of neuropathy. Possible implications of barrier performances for anti-leprosy drug treatment of patients are discussed.This publication has 37 references indexed in Scilit:
- PHYLOGENETIC VARIATIONS IN THE VASCULAR PERMEABILITY OF PERIPHERAL NERVES TO SERUM ALBUMINActa Pathologica Microbiologica Scandinavica, 2009
- Immunocytochemical studies on anti-leprosy drugs in tissuesUltramicroscopy, 1984
- DO ANTI-LEPROSY DRUGS REACH MYOBACTERIUM LEPRAE IN PERIPHERAL NERVES?The Lancet, 1981
- Endothelial Surface Charge: Blood-Brain Barrier Opening to Horseradish Peroxidase Induced by the Polycation Protamin SulfatePublished by Springer Nature ,1981
- Permeability of blood nerve barriers in the diabetic ratJournal of Neurology, Neurosurgery & Psychiatry, 1972
- Studies on vascular permeability in peripheral nervesActa Neuropathologica, 1968
- The distribution within the brain of ferritin injected into cerebrospinal fluid compartments. II. Parenchymal distributionJournal of Anatomy, 1965
- THE USE OF LEAD CITRATE AT HIGH pH AS AN ELECTRON-OPAQUE STAIN IN ELECTRON MICROSCOPYThe Journal of cell biology, 1963
- Prefixation use of hyaluronidase to improve in situ preservation for electron microscopyJournal of Ultrastructure Research, 1958
- Contributions to the Problem of the Peripheral Nervous BarrierActa Medica Scandinavica, 1938