Understanding the causes for the suboptimal long-term graft survival in these patients is fundamental, particularly if such therapies are

to be offered to young patients with an expectation of lifetime benefits. Understanding how transplanted tissue behaves in a severely diseased brain is also of critical importance for the future of stem cell therapy, which will be facing the same challenges. The observations derived from these unique autopsied transplanted HD cases will be invaluable in extending our understanding of HD pathology itself and may very well lead to the improvement and development of cell-based treatments or other similar therapeutic strategies. The authors wish to thank Mr Gilles Chabot for artwork. Both authors were involved in the literature search, the design of tables and schematics as well Smoothened Agonist as in the writing of the manuscript. The authors declare no conflict of interest. “
“H. Madarame, T. Seuberlich, C. Abril, A. Zurbriggen, M. Vandevelde and A. Oevermann (2011) Neuropathology and Applied Neurobiology37, Selleckchem BGB324 753–767 The distribution of E-cadherin expression in listeric rhombencephalitis of

ruminants indicates its involvement in Listeria monocytogenes neuroinvasion Aim: To investigate the expression of E-cadherin, a major host cell receptor for Listeria monocytogenes (LM) internalin A, in the ruminant nervous system and its putative role in brainstem invasion and intracerebral spread of LM in the natural

disease. Methods: Immunohistochemistry and double immunofluorescence was performed on brains, cranial nerves and ganglia of ruminants with and without natural LM rhombencephalitis using antibodies against E-cadherin, protein gene product 9.5, myelin-associated glycoprotein and LM. Results: In the ruminant brain, E-cadherin is expressed in choroid plexus epithelium, meningothelium PI-1840 and restricted neuropil areas of the medulla, but not in the endothelium. In cranial nerves and ganglia, E-cadherin is expressed in satellite cells and myelinating Schwann cells. Expression does not differ between ruminants with or without listeriosis and does not overlap with the presence of microabscesses in the medulla. LM is observed in phagocytes, axons, Schwann cells, satellite cells and ganglionic neurones. Conclusion: Our results support the view that the specific ligand–receptor interaction between LM and host E-cadherin is involved in the neuropathogenesis of ruminant listeriosis. They suggest that oral epithelium and Schwann cells expressing E-cadherin provide a port of entry for free bacteria offering a site of primary intracellular replication, from where the bacterium may invade the axonal compartment by cell-to-cell spread.