Katsuhiro Yamanaka1, Naoto Sasaki2, Yasuyuki Fujita3, Atsuhiko Kawamoto3, Ken-ichi Hirata2, Yutaka Okita4. 1. Division of Cardiovascular Surgery, Department of Surgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-Cho, Chuo-ku, Kobe, 650-0017, Japan. yamakachubanzai@gmail.com. 2. Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan. 3. Unit of Regenerative Medicine, Division of Vascular Regeneration, Institute of Biomedical Research and Innovation Hospital, Chuo-ku, Kobe, Japan. 4. Division of Cardiovascular Surgery, Department of Surgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-Cho, Chuo-ku, Kobe, 650-0017, Japan.
Abstract
OBJECTIVE: The aim of this study was to clarify the impact of acquired and innate immunity on spinal cord ischemia and reperfusion injury using a mouse model of spinal cord ischemia. METHODS: To define the ischemic duration that caused paraplegia, wild-type and severe combined immunodeficiency (SCID) mice were subjected to cross-clamping of the aorta for 7, 9, 9.5, or 10.5 min with ischemic preconditioning for intestinal protection. In wild-type and SCID mice with paraplegia, histological analyses were performed to investigate viable neurons, inflammatory cells, and reactive astrocytes at 12, 24, 48, and 72 h as well as 7 days after reperfusion. RESULTS: In both wild-type and SCID mice, immediate paraplegia was induced by occlusion for 10.5 min. In both wild-type and SCID mice, no infiltration of T or B lymphocytes was observed at any point after reperfusion, but reactive astrocytes were clearly visible at 7 days after reperfusion, and the number of activated microglia peaked at 12 and 48 h after reperfusion. Although there was no significant difference, wild-type mice had a tendency to have more activated microglia than SCID mice at 12 h after reperfusion, and to have less viable neurons than SCID mice at 12, 24, 48, and 72 h after reperfusion. There was a tendency that the frequency of immediate paraplegia in wild-type mice was more than SCID mice though no statistical difference was observed. CONCLUSIONS: Innate immunity, rather than acquired immunity, may be involved in the developing immediate paraplegia in our mouse model.
OBJECTIVE: The aim of this study was to clarify the impact of acquired and innate immunity on spinal cord ischemia and reperfusion injury using a mouse model of spinal cord ischemia. METHODS: To define the ischemic duration that caused paraplegia, wild-type and severe combined immunodeficiency (SCID) mice were subjected to cross-clamping of the aorta for 7, 9, 9.5, or 10.5 min with ischemic preconditioning for intestinal protection. In wild-type and SCIDmice with paraplegia, histological analyses were performed to investigate viable neurons, inflammatory cells, and reactive astrocytes at 12, 24, 48, and 72 h as well as 7 days after reperfusion. RESULTS: In both wild-type and SCIDmice, immediate paraplegia was induced by occlusion for 10.5 min. In both wild-type and SCIDmice, no infiltration of T or B lymphocytes was observed at any point after reperfusion, but reactive astrocytes were clearly visible at 7 days after reperfusion, and the number of activated microglia peaked at 12 and 48 h after reperfusion. Although there was no significant difference, wild-type mice had a tendency to have more activated microglia than SCIDmice at 12 h after reperfusion, and to have less viable neurons than SCIDmice at 12, 24, 48, and 72 h after reperfusion. There was a tendency that the frequency of immediate paraplegia in wild-type mice was more than SCIDmice though no statistical difference was observed. CONCLUSIONS: Innate immunity, rather than acquired immunity, may be involved in the developing immediate paraplegia in our mouse model.
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