C57BL/6 mice are resistant to acute restraint modulation of cutaneous hypersensitivity

C57BL/6 mice, in contrast to BALB/c mice, display minimal behavioral change s in response to environmental stressors and are considered relatively stre ss-resistant. We have shown that application of acute restraint prior to ch emical challenge enhanced cutaneous hypersensitivity (CHS) in BALB/c mice a nd that this enhanced response is partially glucocorticoid dependent. Due t o strain differences in the immune response and in the response to environm ental stressors, we hypothesized that acute restraint would not enhance CHS in the less stress-sensitive C5713L/6 mice. We sensitized and challenged C 5713L/6 mice with the contact sensitizer, 2, 4-dinitrofluorobenzene (DNFB) in the presence and absence of restraint. Acute restraint, applied prior to chemical challenge, significantly increased serum corticosterone, but to c oncentrations approximately 60% of those reported for BALB/c mice. Neither restraint nor the exogenous administration of corticosterone enhanced chemi cal-induced ear swelling in C5713L/6 mice. Pharmacological interruption of the hypothalamic pituitary adrenal axis (HPAA) with the glucocorticoid type II receptor antagonist, RU486, did not alter the development of CHS, howev er, adrenalectomized (ADX) mice exhibited decreased ear swelling, a measure ment that was decreased further by restraint. Combined application of acute restraint and corticosterone prior to chemical challenge significantly enh anced the ear swelling response in C5713L/6 wild-type mice. These data conf irm that C5713L/6 mice have a blunted corticosterone response to restraint and that acute restraint does not modulate cutaneous hypersensitivity. Furt hermore, our data demonstrate that stress-resistance is not conferred exclu sively through the glucocorticoid pathways.