Effects of early experience and differential housing on susceptibility to gastric erosions in lesion-susceptible rats.
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Biomedical subjects
Publications and source records attributed to R Ader.
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An illness-induced taste aversion was conditioned in rats by pairing saccharin with cyclophosphamide, an immunosuppressive agent. Three days after conditioning, all animals were injected with sheep erythrocytes. Hemagglutinating antibody titers measured 6 days after antigen administration were high in placebo-treated rats. High titers were also observed in nonconditioned animals and in conditioned animals that were nor subsequently exposed to saccharin. No agglutinating antibody was detected in conditioned animals treated with cyclophosphamide at the time of antigen administration. Conditioned animals exposed to saccharin at the time of or following the injection of antigen were significantly immunosuppressed. An illness-induced taste aversion was also conditioned using LiCl, a nonimmunosuppressive agent. In this instance, however, there was no attenuation of hemagglutinating antibody titers in response to injection with antigen.
OBJECTIVE: Psychoneuroimmunology, which investigates the bidirectional communication between the central nervous system and the immune system, has been greatly advanced by the use of animal models. The objective of this paper is to describe animal models of disease that can or might be utilized to elucidate neural-immune interactions that alter pathogenesis. METHODS: This paper reviews animal studies that have demonstrated a link among the brain, behavior, immunity, and disease, highlighting models in which the potential contribution of CNS-immune interactions has not yet been explored. RESULTS: Animal studies allow for careful control of environmental stimuli, genetic background, and immunological challenge. As such, they are an important component of psychoneuroimmunology research. Models in which one might study the role of psychosocial factors in immunologically mediated disease processes, as in the case of other pathophysiologic processes, profit from an ability to manipulate both stressful events and the magnitude of the challenge to the immune system. CONCLUSIONS: Animal studies in psychoneuroimmunology highlight the complexity of the interactions among behavior, the brain, the immune system, and pathogen. The genetic background of the animal (both in terms of central nervous and immune system responses), its previous history, the nature of the stressor, the nature of the pathogen and the type of immune response generated are some of the interacting factors that determine the magnitude and direction of stress-induced changes in disease outcome.
OBJECTIVE: The primary objective of the present study was to identify neuroendocrine and immunological correlates of cardiovascular reactivity to an acute laboratory stressor. METHODS: Subjects were 56 healthy volunteers. Heart rate and blood pressure were assessed at regular intervals during a 30-minute adaptation period and a 6-minute videotaped speech task. Blood was drawn before and after the task and was assayed for natural killer cell activity (NKCA), cortisol production, in vitro interferon gamma (IFN-gamma) and interleukin 10 production by peripheral blood mononuclear cells (PBMC), and antibody titers to the Epstein-Barr virus. Psychological measures were also administered. RESULTS: NKCA increased significantly in response to the task, and this increase was significantly and positively correlated with heart rate reactivity. IFN-gamma production by PBMC also increased in response to the task, but these increases were unrelated to heart rate reactivity. In addition, baseline cortisol levels were found to be predictive of heart rate reactivity. Finally, questionnaire data were modestly related to various aspects of stress-induced reactivity. CONCLUSIONS: Consistent with the task-related increases in NKCA and IFN-gamma, acute stress may signal an increase in at least some aspects of the cell-mediated, or TH1-driven, immune response. Furthermore, the finding that heart rate reactivity was related in part to baseline individual differences in cortisol production suggests that short-term cardiovascular responses to stress may be directly related to longer-term neuroendocrine modulation. Finally, the present results also help to highlight the influence of both sympathetic and nonsympathetic pathways in the response to acute stressors and suggest tentative links between certain psychological traits and various aspects of stress-induced reactivity.
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