CHEM STUDY OF NATL KILLER CELL TOX FOLLOWING SURG STRESS
CHEM STUDY OF NATL KILLER CELL TOX FOLLOWING SURG STRESS
批准号:
3079404
负责人:
RAPHAEL E. POLLOCK
金额:
$7.62万
依托单位国家:
美国
项目类别:
财政年份:
1984
资助国家:
美国
项目状态:
已结题
起止时间:
1984-04-15 至 1989-03-31
关键词:
中文摘要
自然杀伤细胞(NKCC)对肿瘤的杀伤作用可能是有效的
英文摘要
Natural killer cell cytotoxicity (NKCC) against tumor may be
important in preventing in vivo solid tumor dissemination.
Multiple animal models demonstrate increased rates of tumor
dissemination after surgical stress; previously we have observed
that surgical stress impairs murine NKCC. Because of the
importance of surgery in the control of solid tumor it may be
valuable to examine the mechanism underlying surgical stress
impairment of NKCC. Result of this research demonstrate that
post surgical suppression of NKCC began as early as 2 hr after
murine hind limb amputation, reached nadir at 4 days, and did not
recover to control level until postoperative day 23. Anesthetic
treatment alone did not cause comparable NKCC suppression.
The suppression of NKCC accompanied changes in both splenic
size and morphology. The immune suppression was observed in
multiple compartments, including peripheral blood, bone marrow,
and spleen. Mixing experiments demonstrated that surgical stress
per se generated a suppressor cell population affecting NKCC;
calibrated bleeding did not generate comparable suppression of
NKCC. The observed suppression apparently required cell-to-cell
contact since supernatants from 4 and 18 hr cultures of suppressor
cells did not cause suppression. The observed suppression was
prevented by perioperative treatment with the interferon inducing
pyrimdinone analog 2-amino-5-bromo-6-phenyl-4-pyrimidinol
(ABPP). These preclinical observations point to the future of NK
specific perioperative immunotherapy that may help prevent
possible tumor dissemination from occurring at the time of
surgery.
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