Examination of the neuroendocrine basis for the social conflict-induced enhancement of immunity in mice.

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 beta-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 beta-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.