Psychosocial stress augments tumor development through β-adrenergic activation in mice

Housing conditions affect behavioral and biological responses of animals. We investigated the effect of same-sex-grouped (G), crowded (GC) and isolated (1) conditions on the growth of B16 melanoma or Meth A fibrosarcoma implanted in the footpad of syngeneic male C57BL/6 or BALB/c mice. Differential housing altered host resistance to tumor growth. The host responses to stress were reflected in thymic atrophy, which was lowest in the G mice, highest in the GC mice and intermediate in the I mice. The GC condition was a more stressful social: environment than the I condition in both male C57BL/6 and BALB/c mice. Reflecting the extent of psychosocial stress, tumor growth was augmented in the order of GC, I and G condition, and a negative mass correlation between tumor and thymus was observed, thus clearly indicating that the host resistance to tumors was attenuated by psychosocial stress. Furthermore, the stress-enhanced tumor growth and thymus atrophy were completely abrogated by the oral administration of the non-selective beta-adrenergic antagonist, propranolol. On the contrary, the chronic administration of corticosterone significantly induced the atrophy of thymus and spleen without affecting tumor growth. These results suggest an interrelationship among psychosocial stress, tumor growth and beta-adrenergic activation.