TY - JOUR
T1 - Olfactory receptor neurons prevent disseminations of neurovirulent influenza A virus into the brain by undergoing virus-induced apoptosis
AU - Mori, Isamu
AU - Goshima, Fumi
AU - Imai, Yoshinori
AU - Kohsaka, Shinichi
AU - Sugiyama, Tsuyoshi
AU - Yoshida, Tomoaki
AU - Yokochi, Takashi
AU - Nishiyama, Yukihiro
AU - Kimura, Yoshinobu
PY - 2002/9
Y1 - 2002/9
N2 - Olfactory receptor neurons (ORNs) were infected upon intranasal inoculation with the R404BP strain of neurovirulent influenza A virus. Virus-infected neurons and a small fraction of neighbouring uninfected neurons displayed apoptotic neurodegeneration substantiated by the immunohistochemistry for activated caspase-3 molecules and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling method. However, virus infection was restricted within the peripheral neuroepithelium and all mice survived the infection. Virus-infected ORNs revealed upregulated expression of the Fas ligand molecules, activating the c-Jun N-terminal kinase signal transduction pathway. In addition, Iba 1-expressing activated microglia/macrophages appeared to partake in phagocytic activities, eventually clearing apoptotic bodies. These results raise the possibility that induction of apoptosis in olfactory receptor neurons at an early stage of infection may provide protective effects against invasion of the neurovirulent virus from the peripheral to the CNS.
AB - Olfactory receptor neurons (ORNs) were infected upon intranasal inoculation with the R404BP strain of neurovirulent influenza A virus. Virus-infected neurons and a small fraction of neighbouring uninfected neurons displayed apoptotic neurodegeneration substantiated by the immunohistochemistry for activated caspase-3 molecules and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling method. However, virus infection was restricted within the peripheral neuroepithelium and all mice survived the infection. Virus-infected ORNs revealed upregulated expression of the Fas ligand molecules, activating the c-Jun N-terminal kinase signal transduction pathway. In addition, Iba 1-expressing activated microglia/macrophages appeared to partake in phagocytic activities, eventually clearing apoptotic bodies. These results raise the possibility that induction of apoptosis in olfactory receptor neurons at an early stage of infection may provide protective effects against invasion of the neurovirulent virus from the peripheral to the CNS.
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U2 - 10.1099/0022-1317-83-9-2109
DO - 10.1099/0022-1317-83-9-2109
M3 - Article
C2 - 12185263
AN - SCOPUS:0036711686
SN - 0022-1317
VL - 83
SP - 2109
EP - 2116
JO - Journal of General Virology
JF - Journal of General Virology
IS - 9
ER -