Examination of the neuroendocrine basis for the social conflict-induced enhancement of immunity in mice.
Examination of the neuroendocrine basis for the social conflict-induced enhancement of immunity in mice.
复制标题
检查社会冲突引起的小鼠免疫力增强的神经内分泌基础。
DOI：
10.1016/0031-9384(90)90212-m
复制
发表时间：
1990
影响因子：
2.9
通讯作者：
Baissa,B
中科院分区：
文献类型：
--
作者：
Lyte,M;Nelson,SG;Baissa,B
Intruder DBA/2 and C57BL/6 mice, which display different neuroendocrine responses to social conflict, evidence a pronounced increase in splenocyte phagocytosis of opsonized zymosan particles as a consequence of social conflict-induced stress. Interruption of the hypothalamic-pituitary-adrenal axis prior to social conflict results in an abrogation of the stress-induced enhancement of phagocytosis in DBA/2, but not in C57BL/6, mice. Administration of the opiate antagonists naloxone and naltrexone resulted in a potentiation of the stress-induced enhancement of phagocytosis in both strains. Similarly, administration of the alkylating antagonist β-chlornaltrexamine which irreversibly blocks opioid binding sites potentiated the immune-enhancing effects of social conflict stress. Mitogen-induced T and B lymphocyte proliferation was unaffected by any of the experimental procedures with the exception of β-chlornaltrexamine which suppressed activity equally in stressed and nonstressed groups. These results demonstrate the necessity of employing inbred murine strains in the dissection of the neuroendocrine pathways which govern stress-induced modulation of the immune system.
