title: A differential response to stress is not a prediction of susceptibility or severity in adjuvant-induced arthritis.
abstract: It has been suggested that glucocorticoid insufficiency consequent to a blunted hypothalamo-pituitary-adrenal (HPA) axis response to stress may be associated with increased susceptibility to certain experimentally induced autoimmune diseases. We have developed a model which allows this hypothesis to be tested within a single population of rats, using the open field stress. Following the open field stress, rats were divided into groups of high or low emotivity on the basis of faecal pellet count. High and low emotivity groups exhibited significantly elevated plasma corticosterone following the open field stress compared to pre-stress levels, but the corticosterone response of the low emotivity rats was significantly lower than that of the high emotivity rats (p < 0.01). Four hours following termination of the stress, groups of high or low emotivity rats were further divided into two groups and given either an intradermal injection of Mycobacterium butyricum or vehicle for the induction of arthritis. Fourteen days after injection of adjuvant, paw volumes in the arthritic high and low emotivity groups were significantly greater than their respective vehicle-injected non-arthritic controls. However, in spite of the differential corticosterone response to stress, there was no significant difference in paw volumes between the arthritic high and low emotivity groups. These data show that an attenuated response to stress is not associated with enhanced susceptibility to the inflammatory disease of adjuvant-induced arthritis, or with increased severity of inflammation as measured by paw volume on day 14. This experimental paradigm can be more widely applied to extend our observations on the relationship between the HPA axis response to stress and susceptibility to inflammation in other models of experimentally induced autoimmune disease.
authors.affiliation: Department of Neurosciences, University of Cadiz, Spain; Division of Medicine, University of Bristol, UK; The Panum Institute, University of Copenhagen, Denmark.
authors.forename: A J
authors.initials: AJ
authors.lastname: Chover-Gonzalez
authors.forename: P
authors.initials: P
authors.lastname: Tejedor-Real
authors.forename: M S
authors.initials: MS
authors.lastname: Harbuz
authors.forename: J
authors.initials: J
authors.lastname: Gibert-Rahola
authors.forename: P J
authors.initials: PJ
authors.lastname: Larsen
authors.forename: D S
authors.initials: DS
authors.lastname: Jessop
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000503:physiopathology* / Q000523:psychology; D003345:Corticosterone / Q000097:blood*; D004198:Disease Susceptibility; D004487:Edema; D004644:Emotions; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D009161:Mycobacterium / Q000276:immunology; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013315:Stress, Psychological / Q000276:immunology / Q000503:physiopathology*
chemical_list: D003345:Corticosterone