Does the Hypothalamus-Pituitary-Adrenal axis play a role in the immune response to gastrointestinal nematodes?

The aim of this study was to establish a model for examining the role of the neuroendocrine system in regulating the immune response of the host to gastrointestinal nematodes. Through this model the role of the neuroendocrine system in responding to parasitism and regulating the T Helper 2 (TH2) response was investigated. Specifically, Fischer and Lewis rats were used to discover whether differing, but physiological glucocorticoid levels altered the response to parasites. In addition, a cell culture model was used to examine the interaction between parasites and dexamethasone in epithelial cell gene expression. Results showed that whilst gene expression patterns differed between the two rat strains, the key responses in the immune and gastro-intestinal systems did not differ. Both rat strains mounted an effective response to parasites, blocking the lifecycle before adult, egg laying nematodes could develop. In contrast, the addition of high levels of dexamethasone in a cell-culture model changed cellular gene expression responses to parasitism significantly. Results suggest that immune responses can remain effective despite marked changes in physiological glucocorticoid levels, but that artificial glucocorticoid administration can exceed a threshold above which significant immunosuppression can occur. Intriguingly, gene expression responses to parasitism were observed in brain tissues and adrenal glands providing a glimpse of the capacity for signals to be transmitted from the site of parasitism by the neuro-endocrine system.