Social conflict has been shown to affect the neuroendocrine stress response
s in rodents. The current study was designed to characterize the effects of
social conflict on leukocyte subset distribution and function as well as i
n vivo bacterial growth. Male DBA/2 mice implanted or not implanted with a
closed chamber containing Escherichia coli were repeatedly challenged by te
mporary placement in the territory of a dominant CF-1 mouse five times a da
y for 2 consecutive days. Nonstressed animals were similarly handled, but w
ere not exposed to social conflict. Effects on immune responses and E. coli
growth were analyzed 13 h after the last social conflict session. Social c
onflict alone was associated with an increase in plasma corticosterone conc
entration and decreases in thymocyte numbers and splenocyte ability to prol
iferate in vitro in the presence of lipopolysaccharide (p < 0.05). After so
cial conflict, immature CD4+ CD8+ thymocytes decreased, whereas mature T ce
lls increased (p < 0.05). In the presence of E. coli, social conflict induc
ed a significant increase in plasma concentration of interleukin-1 beta, an
d a decrease in the number of thymocytes and the percentage of CD4+ Cd8+ T
cells in the thymus (p < 0.05). In addition to the lymphocyte subpopulation
changes observed with social conflict alone, the proportion of CD3+ and ma
jor histocompatability complex (MHC) class II IA(d)+ cells were significant
ly higher in stressed mice implanted with a closed chamber containing E. co
li (p < 0.05). Social conflict tended to favor E. coli growth in the closed
chamber, indicating possible direct bacterial-neuroendocrine hormone inter
actions. Taken together, these results suggest that stress may modulate the
host immune response by altering both bacterial growth and resistance to i
nfection. (C) 1999 Elsevier Science Inc.