title: Effects of social conflict on immune responses and E. coli growth within closed chambers in mice.
abstract: Social conflict has been shown to affect the neuroendocrine stress response in rodents. The current study was designed to characterize the effects of social conflict on leukocyte subset distribution and function as well as in vivo bacterial growth. Male DBA/2 mice implanted or not implanted with a closed chamber containing Escherichia coli were repeatedly challenged by temporary placement in the territory of a dominant CF-1 mouse five times a day for 2 consecutive days. Nonstressed animals were similarly handled, but were not exposed to social conflict. Effects on immune responses and E. coli growth were analyzed 13 h after the last social conflict session. Social conflict alone was associated with an increase in plasma corticosterone concentration and decreases in thymocyte numbers and splenocyte ability to proliferate in vitro in the presence of lipopolysaccharide (p < 0.05). After social conflict, immature CD4+CD8+ thymocytes decreased, whereas mature T cells increased (p < 0.05). In the presence of E. coli, social conflict induced a significant increase in plasma concentration of interleukin-1beta, and 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 major histocompatibility complex (MHC) class II IAd+ cells were significantly higher in stressed mice implanted with a closed chamber containing E. coli (p < 0.05). Social conflict tended to favor E. coli growth in the closed chamber, indicating possible direct bacterial-neuroendocrine hormone interactions. Taken together, these results suggest that stress may modulate the host immune response by altering both bacterial growth and resistance to infection.
authors.affiliation: Department of General Surgery Research, Carolinas Medical Center, Charlotte, NC 28203, USA. ddreau@carolinas.org
authors.forename: D
authors.initials: D
authors.lastname: Dréau
authors.forename: G
authors.initials: G
authors.lastname: Sonnenfeld
authors.forename: N
authors.initials: N
authors.lastname: Fowler
authors.forename: D S
authors.initials: DS
authors.lastname: Morton
authors.forename: M
authors.initials: M
authors.lastname: Lyte
mesh_terms: D000818:Animals; D001143:Arousal / Q000502:physiology*; D016516:CD4-CD8 Ratio; D015169:Colony Count, Microbial; D003220:Conflict, Psychological; D003345:Corticosterone / Q000097:blood; D004291:Dominance-Subordination; D019453:Escherichia coli O157 / Q000254:growth & development / Q000276:immunology*; D007108:Immune Tolerance / Q000276:immunology; D007375:Interleukin-1 / Q000097:blood; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D008815:Mice, Inbred Strains; D012884:Skin Window Technique; D013045:Species Specificity
chemical_list: D007375:Interleukin-1; D003345:Corticosterone