Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats
High blood levels of inflammatory biomarkers and immune cells in stroke lesions have been recognized as results of stroke. However, recent studies have suggested that inflammation occurs prior to stroke onset. In this study, we aimed to clarify the role of inflammation in stroke onset among stroke-p...
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Wiley
2012-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2012/701976 |
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author | Tsuyoshi Chiba Tatsuki Itoh Masaki Tabuchi Toru Nakazawa Takao Satou |
author_facet | Tsuyoshi Chiba Tatsuki Itoh Masaki Tabuchi Toru Nakazawa Takao Satou |
author_sort | Tsuyoshi Chiba |
collection | DOAJ |
description | High blood levels of inflammatory biomarkers and immune cells in stroke lesions have been recognized as results of stroke. However, recent studies have suggested that inflammation occurs prior to stroke onset. In this study, we aimed to clarify the role of inflammation in stroke onset among stroke-prone spontaneously hypertensive rats (SHRSP). At 4 weeks of age (before stroke onset), the plasma level of IL-1β was significantly higher in SHRSP (153.0±49.7 pg/ml) than in Wistar Kyoto rats (WKY) (7.7±3.4 pg/ml, P<0.001 versus SHRSP) or spontaneously hypertensive rats (SHR) (28.0±9.1 pg/ml, P<0.001 versus SHRSP) (n=6 per strain). Stimulated IL-1β signal was also observed in cerebrovascular endothelial cells of SHRSP. Gene expressions of IL-1β, IL-1 receptors, caspase-1, and downstream genes (MCP-1 and ICAM-1), which associated with immune cell recruitment, were significantly greater in SHRSP than in WKY or SHR, coincident with greater NFκB protein levels in SHRSP compared to WKY or SHR. In addition, continuous administration of IL-1β (2 μg/day) using an osmotic pump slightly increased the incidence of stroke in SHR (P=0.046) and significantly accelerated the onset of stroke in SHRSP (P=0.006) compared to each control (n=10 per group). These results suggest that a stimulated IL-1β signal might be a cause of stroke onset when concomitant with severe hypertension. |
format | Article |
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institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2012-01-01 |
publisher | Wiley |
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spelling | doaj-art-de29dcb428d74fea82d03167403be8932025-02-03T01:07:30ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/701976701976Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive RatsTsuyoshi Chiba0Tatsuki Itoh1Masaki Tabuchi2Toru Nakazawa3Takao Satou4Information Center, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8636, JapanDepartment of Pathology, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-sayama, Osaka 589-8511, JapanDepartment of Biochemistry, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-sayama, Osaka 589-8511, JapanFirst Institute of New Drug Discovery, Otsuka Pharmaceutical Co., Ltd., Tokushima 771-0192, JapanDepartment of Pathology, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-sayama, Osaka 589-8511, JapanHigh blood levels of inflammatory biomarkers and immune cells in stroke lesions have been recognized as results of stroke. However, recent studies have suggested that inflammation occurs prior to stroke onset. In this study, we aimed to clarify the role of inflammation in stroke onset among stroke-prone spontaneously hypertensive rats (SHRSP). At 4 weeks of age (before stroke onset), the plasma level of IL-1β was significantly higher in SHRSP (153.0±49.7 pg/ml) than in Wistar Kyoto rats (WKY) (7.7±3.4 pg/ml, P<0.001 versus SHRSP) or spontaneously hypertensive rats (SHR) (28.0±9.1 pg/ml, P<0.001 versus SHRSP) (n=6 per strain). Stimulated IL-1β signal was also observed in cerebrovascular endothelial cells of SHRSP. Gene expressions of IL-1β, IL-1 receptors, caspase-1, and downstream genes (MCP-1 and ICAM-1), which associated with immune cell recruitment, were significantly greater in SHRSP than in WKY or SHR, coincident with greater NFκB protein levels in SHRSP compared to WKY or SHR. In addition, continuous administration of IL-1β (2 μg/day) using an osmotic pump slightly increased the incidence of stroke in SHR (P=0.046) and significantly accelerated the onset of stroke in SHRSP (P=0.006) compared to each control (n=10 per group). These results suggest that a stimulated IL-1β signal might be a cause of stroke onset when concomitant with severe hypertension.http://dx.doi.org/10.1155/2012/701976 |
spellingShingle | Tsuyoshi Chiba Tatsuki Itoh Masaki Tabuchi Toru Nakazawa Takao Satou Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats Mediators of Inflammation |
title | Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats |
title_full | Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats |
title_fullStr | Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats |
title_full_unstemmed | Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats |
title_short | Interleukin-1β Accelerates the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats |
title_sort | interleukin 1β accelerates the onset of stroke in stroke prone spontaneously hypertensive rats |
url | http://dx.doi.org/10.1155/2012/701976 |
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