송아지 56마리의 부검 실험을 통해 광우병 변형 프리온이 자율신경계를 통해서 창자로부터 중추신경계(뇌)로 이동한다는 사실을 규명한 논문입니다.
변형프리온은 2가지 경로를 통해 위장관(gastrointestinal tract, GIT) 으로부터 중추신경계로 (central nervous system, CNS)로 이동하는데… 교감신경 및 부교감신경경로 2가지의
자율신경계 경로를 통하는 것으로 추정하고 있습니다.
( i) via the coeliac and mesenteric ganglion complex, splanchnic nerves and the lumbal/caudal thoracic spinal cord (representing the sympathetic GIT innervation);
(ii) via the Nervus vagus (parasympathetic GIT innervation). The dorsal root ganglia seem to be subsequently affected, so it is likely that BSE prion invasion of the non-autonomic peripheral nervous system (e.g. sciatic nerve) is a secondary retrograde event following prion replication in the CNS.
특히 이 연구에서는 2007년까지 알려진 것보다 8개월이나 빠른 시기인 접종 후 24개월(28개월령으로 추정) 후에 중추신경, 말초신경, 회장에서 광우병 원인체인 변형 프리온이 검출되었다고 보고하고 있습니다.
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J Gen Virol. 2007 Mar;88(Pt 3):1048-55.
Prions spread via the autonomic nervous system from the gut to the central nervous system in cattle incubating bovine spongiform encephalopathy.
Hoffmann C, Ziegler U, Buschmann A, Weber A,
Kupfer L, Oelschlegel A, Hammerschmidt B, Groschup MH.
Abstract
To elucidate the still-unknown pathogenesis of bovine spongiform encephalopathy (BSE), an oral BSE challenge and sequential kill study was carried out on 56 calves. Relevant tissues belonging to the peripheral and central nervous system, as well as to the lymphoreticular tract, from necropsied animals were analysed by highly sensitive immunohistochemistry and immunoblotting techniques to reveal the presence of BSE-associated pathological prion protein (PrPSc) depositions. Our results demonstrate two routes involving the autonomic nervous system through which BSE prions spread by anterograde pathways from the gastrointestinal tract (GIT) to the central nervous system (CNS): (i) via the coeliac and mesenteric ganglion complex, splanchnic nerves and the lumbal/caudal thoracic spinal cord (representing the sympathetic GIT innervation); and (ii) via the Nervus vagus (parasympathetic GIT innervation). The dorsal root ganglia seem to be subsequently affected, so it is likely that BSE prion invasion of the non-autonomic peripheral nervous system (e.g. sciatic nerve) is a secondary retrograde event following prion replication in the CNS. Moreover, BSE-associated PrPSc was already detected in the brainstem of an animal 24 months post-infection, which is 8 months earlier than reported previously. These findings are important for the understanding of BSE pathogenesis and for the development of new diagnostic strategies for this infectious disease.
