Oldham G, Bridger J C
Division of Immunology and Pathology, AFRC Institute for Animal Health, Compton Laboratory, UK.
Vet Immunol Immunopathol. 1992 Apr;32(1-2):77-92. doi: 10.1016/0165-2427(92)90070-7.
Rotavirus-naive and rotavirus-immune gnotobiotic calves were treated with high doses of dexamethasone (DX) to suppress the immune system. Calves were then infected with a virulent rotavirus inoculum, J-160, to investigate the role of immune responses both in recovery from primary rotavirus infection and in resistance to secondary rotavirus infection. Treatment of calves with DX markedly suppressed in vitro responsiveness of peripheral blood lymphocytes to mitogens within 48 h of the start of DX treatment. Suppression was similar in rotavirus-naive and rotavirus-immune calves. In contrast, the effect of DX treatment on specific antibody responses differed depending on when DX treatment started in relation to rotavirus infection. When DX treatment commenced prior to primary rotavirus infection both systemic and local specific antibody responses were inhibited. These calves, in which mitogen and antibody responses were suppressed, exhibited greater clinical signs than did control calves after infection with virulent rotavirus, but virus excretion was affected in only one of the two calves. When DX treatment was started after primary rotavirus infection but before secondary infection, systemic and local antibody responses to the primary infection and to the challenge infection were not affected. These calves resisted challenge with virulent virus as did DX-untreated rotavirus-immune calves, even though mitogen responses were suppressed. We conclude that in a primary rotavirus infection, virus excretion ceased when both antibody and mitogen responses were suppressed. Resistance to secondary rotavirus infection occurred when mitogen responsiveness was suppressed, but when antibody levels were normal. Thus, no evidence was obtained that fully functional cell-mediated immune mechanisms are essential for resistance to rotavirus infection. Evidence was provided for the ability of parenteral treatment with DX to suppress mucosal as well as systemic antibody responses.
将新生且未感染轮状病毒以及已感染轮状病毒并具有免疫力的无菌小牛用高剂量地塞米松（DX）进行处理，以抑制其免疫系统。随后，给这些小牛接种强毒性轮状病毒接种物J - 160，以研究免疫反应在原发性轮状病毒感染恢复以及对继发性轮状病毒感染的抵抗力中的作用。在开始DX处理后的48小时内，用DX处理小牛显著抑制了外周血淋巴细胞对有丝分裂原的体外反应性。在新生且未感染轮状病毒以及已感染轮状病毒并具有免疫力的小牛中，抑制情况相似。相比之下，DX处理对特异性抗体反应的影响取决于DX处理相对于轮状病毒感染开始的时间。当在原发性轮状病毒感染之前开始DX处理时，全身和局部特异性抗体反应均受到抑制。这些有丝分裂原和抗体反应受到抑制的小牛，在感染强毒性轮状病毒后，比对照小牛表现出更明显的临床症状，但在两只小牛中只有一只的病毒排泄受到影响。当在原发性轮状病毒感染后但在继发性感染之前开始DX处理时，对原发性感染和激发感染的全身和局部抗体反应均未受到影响。这些小牛对强毒性病毒的激发具有抵抗力，就像未用DX处理的已感染轮状病毒并具有免疫力的小牛一样，尽管有丝分裂原反应受到抑制。我们得出结论，在原发性轮状病毒感染中，当抗体和有丝分裂原反应均受到抑制时，病毒排泄停止。当有丝分裂原反应性受到抑制但抗体水平正常时，对继发性轮状病毒感染产生抵抗力。因此，没有证据表明功能完全正常的细胞介导免疫机制对于抵抗轮状病毒感染至关重要。有证据表明，经肠道外给予DX能够抑制黏膜以及全身抗体反应。
