1990 Fiscal Year Final Research Report Summary
Modulatory Effect of Dietary Restriction on the Advance of Senescence in Senescence Accelerated Mouse (SAM)
| Project/Area Number |
01480165
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TAKEDA Toshio Kyoto Univ., Chest Dis. Research Institute, Professor, 胸部疾患研究所, 教授 (00027088)
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| Co-Investigator(Kenkyū-buntansha) |
HIGUCHI Keiichi Kyoto Univ., Chest Dis. Res. Institute, Lecturer, 胸部疾患研究所, 講師 (20173156)
HOSOKAWA Masanori Kyoto Univ., Chest Dis. Res. Institute, Associate Professor, 胸部疾患研究所, 助教授 (00127135)
HOSONO Masamichi Kyoto Univ., Chest Dis. Res. Institute, Associate Professor, 胸部疾患研究所, 助教授 (90107433)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Senescence Accelerated Mouse / calorie restriction / immune responsiveness / modulation of aging / auto-antibody |
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| Research Abstract |
1. The effects of age and dietary restriction on immune response were investigated using an animal model of accelerated senescence, SAM. Spleen weight and total number of splenic cells were significantly lower in the food-restricted group (fed 60% of energy intake of ad libitum fed) at 8 mo of age. Percentages of T and B cells in the splenic cells were not significantly different between the two groups. The number of direct hemolytic plaqueforming cells per 10^6 spleen cells 4 d following immunization with SRBC and DNP-Ficoll was significantly greater in the 8-mo-old mice in the food-restricted group than in the control (ad libitum fed) group. Mitogen responses to concanavalin A and LPS were maintained in the food-restricted group but were depressed in the control group at 8 mo. In addition, though autoantibody to single-stranded DNA increased in the control group with advancing age, there was a steady decrease in the food-restricted group until 8 mo. Therefore, our results suggest that when SAM are subjected to food restriction, there may be a modulatory effect on te immune dysfunction associated with advancing age.
2. After crossing with high responders, Blo. BR mice, about 12% of (Blo.BR SAM-P/1) (BRP) F_2 mice showed low responsiveness, as did SAM-P/1 mice, against two T-dependent antigens, SRBC and HRBC. Based on the incidence of the low responders in F_2 generation and statistical analyses, tehyporesponsiveness was postulated to be controlled by two genes. To survey the location of these genes, linkage analyses were performed in the F_2 mice using a large set of genetic markers. These results suggest that one of genes controlling the hyporesponsiveness of SAM-P/1 mice is linked t both Gpi-1 and c loci and that it locates at a more proximal site on Chr. /.
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