Stress and Immune Responses IV. Adrenal Involvement in the Alteration of Antibody Responses in Restraint-Stressed Mice

Abstract

Abstract-We investigated the correlation between restraint stress-induced alter ation of antibody responses and adrenal hormones. Adrenalectomy (Adx) blocked both the suppression of antibody response against T cell-dependent (TD) antigen and the enhancement of that against T cell-independent (TI) antigen in stressed mice. Adx also inhibited the atrophy of both thymus and spleen caused by restraint. Pre-treatment of metyrapone, an inhibitor of adrenocortical steroid biosynthesis, had an effect that was similar to, but far weaker than that of Adx on stressed mice. The pre-administration of phenoxybenzamine, an a-adrenergic blocking agent, to mice prevented both the inhibition of antibody response to TD antigen and the decrease in spleen cell number of restrained mice. A similar effect was observed in mice pre-treated with 6-hydroxydopamine, an adrenergic neuron degenerating agent.However, no effects of these two agents were observed on the enhancement of antibody response to TI antigen. The suppressive effect of the antibody response to TD antigen was augmented by the pre-administration of propranolol, a e3-adrenergic blocking agent. These results suggest that the suppression of the function of T cells in restrained mice are attributed to the released adrenocortical and adrenal medullary hormones and activated sympathetic nervous system and that the enhance ment of B cell function is due to the adrenocortical hormones.

Stressor-lnduced Alterations of Immune Function: Mechanisms and Issues

“…However, in another study involving exposure of Swiss-Webster mice to rotation stress (10 min/h for 5 h), ADX did not influence the stressor-induced suppression of the PFC response to SRBC [86]. The discrepancy between this last finding and those cited previously [84,85] may be due to differences in the stressors used, as well as the dura tion of exposure to the stress.…”

“…Okimura et al [84] exposed ADX or sham-ADX BALB/c mice to 2 days of restraint (12 h/day), at the end of which they were immunized with SRBC. The suppressed PFC response to SRBC in sham-restrained mice was totally abrogated by ADX [84], Similarly, Bonneau et al [85] found that exposure of ADX male C57BL/6 mice to 4 days of restraint (14-16 h/day) prior to footpad inoculation with herpes simplex virus type I (HSV-1), followed by an addi tional 5 days of restraint, resulted in an abrogation of sup pressed HSV-specific cytotoxic T lymphocyte (CTL) activ ity observed in sham surgery or unoperated controls ex posed to the same restraint protocol. These findings suggest that some of the effects o f restraint on antigen-specific im mune responses in mice are mediated by adrenal-dependent mechanisms.…”

Immunosuppressive Effect of Restraint Stress on the Initiation of Allergic Rhinitis in Mice

“…A wide range of immunological, endocrinological and neuronal pathways are known to mediate and modulate systemic stress responses [30, 31, 32]. Okimura et al [31], for example, reported that stress-induced production of antibody was stopped by extirpation of the suprarenal glands.…”

“…Okimura et al [31], for example, reported that stress-induced production of antibody was stopped by extirpation of the suprarenal glands. Various studies have also revealed that plasma levels of catecholamines, corticosterone and ACTH are increased by the application of restraint stress [33, 34].…”

Administração de dehidroepiandrosterona (DHEA) como mediador da resposta imune em ratos Wistar infectados com Trypanosoma cruzi submetidos ao estresse repetitivo

“…Os glicocorticóides regulam uma escala de processos biológicos, tais como, proliferação de células, inflamação, imunidade e a diminuição na ativação de células natural Killer (NK) (IWAKABE et al, 1998;SAPERSTEIN et al, 1992;WU et al, 2000), supressão na fagocitose de macrófagos (LU et al, 1998), a liberação de óxido nítrico (NO) e TNF-α (AARSTAD et al, 1991;BROWN & ZWILLING, 1994;KIZAKI et al, 1996), alterando a sensibilidade do IFN-γ (ZWILLING et al, 1992), inibindo a proliferação de células T, produzindo IL-2 e IFN-γ (IWAKABE et al, 1998;LI et al,1997), modulando a expressão MHC de classe II (ZWILLING et al, 1990), efetuando o equilíbrio de células T do tipo 1 e 2 (Th1/Th2) (IWAKABE et al, 1998), e modulando a produção de anticorpos (FUKUI et al, 1997;KOMORI et al, 1996;OKIMURA et al, 1986). É bem aceitável que, a suscetibilidade à infecção e a defesa do hospedeiro contra a invasão de patógenos pode ser alterada em conseqüência aos efeitos de modulação do estresse sobre a resposta imune (BIONDI & ZANNINO, 1997;YANG & GLASER, 2000).…”