| 結束日期 |
2012-03-31 |
| 計畫單位 |
醫學院醫學系學士班微生物學科 |
| 計畫主持人 |
李哲欣(Lee, Che-Hsin) |
| 摘要 |
Systemic administration of Salmonella to tumor-bearing mice leads to the preferential accumulation
within tumor sites and retardation the tumor growth. However, the detailed mechanism of the
Salmonella-induced antitumor immune response via host T cell remained uncertain. Herein, we
used wild-type, CD4+ T-cell-deficient, and CD8+ T-cell-deficient mice to study the role of T cell in
the antitumor immune responses induced by Salmonella enterica serovar Choleraesuis (S.
Choleraesuis).When systemically administered into mice bearing tumors, S. Choleraesuis
significantly inhibited tumor growth by 50%. By contrast, in T-cell-deficient mice, there was only
34%~42% in inhibition of tumor growth.We found that the treatment of S. Choleraesuis
significantly upregulate interferon-γin wild-type and CD8+ T-cell-deficient mice, but not in CD4+
T-cell-deficient mice. Furthermore, immunohistochemical staining of the tumors revealed more
infiltration of macrophages, and neutrophils in wild-type mice after S. Choleraesuis treatment
compared with those in T-cell-deficient mice. The antitumor therapeutic effect mediated by S.
Choleraesuis is associated with an inflammatory immune response at tumor site and a tumor T
helper 1-type immune response. In conclusion, these results suggest that tumor-targeted therapy
using S. Choleraesuis, which exerts tumoricidal effects and stimulates T cell activities, represents a
potential strategy for the treatment of tumor. |
| 關鍵字 |
T cell; Salmonella enterica serovar Choleraesuis; interferon-γ; tumor. |
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