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Endocrine Perturbation Increases Susceptibility of Mice to Anthrax Lethal Toxin

机译：内分泌扰动增加了小鼠对炭疽致死毒素的敏感性

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Bacillus anthracis lethal toxin (LT) causes vascular collapse and high lethality in BALB/cJ mice, intermediate lethality in C57BL/6J mice, and no lethality in DBA/2J mice. We found that adrenalectomized (ADX) mice of all three strains had increased susceptibility to LT. The increased susceptibility of ADX-DBA/2J mice was not accompanied by changes in their macrophage sensitivity or cytokine response to LT. DBA/2J mice showed no change in serum corticosteroid levels in response to LT injection, while BALB/cJ mice showed a fivefold increase in serum corticosterone. However, LT inhibited dexamethasone (DEX)-induced glucocorticoid receptor gene activation to similar extents in all three strains. DEX treatment did not rescue ADX mice from LT-mediated mortality. Surprisingly, oral DEX treatment also sensitized adrenally intact DBA/2J mice to LT lethality at all doses tested and also exacerbated LT-mediated pathogenesis and mortality in BALB/cJ mice. Aldosterone did not protect ADX mice from toxin challenge. These results indicate that susceptibility to anthrax LT in mice depends on a fine but easily perturbed balance of endocrine functions. Thus, the potentially detrimental consequences of steroid therapy for anthrax must be considered in treatment protocols for this disease.
机译：炭疽杆菌致死毒素（LT）在BALB / cJ小鼠中引起血管萎缩和高致死性，在C57BL / 6J小鼠中引起中等致死性，而在DBA / 2J小鼠中没有致死性。我们发现所有这三个品系的肾上腺切除术（ADX）小鼠对LT的敏感性增加。 ADX-DBA / 2J小鼠的易感性增加并未伴随巨噬细胞敏感性或对LT的细胞因子反应的改变。 DBA / 2J小鼠对LT注射后血清皮质类固醇水平无变化，而BALB / cJ小鼠血清皮质类固醇水平增加5倍。但是，LT在所有三个菌株中都以相似的程度抑制了地塞米松（DEX）诱导的糖皮质激素受体基因的激活。 DEX处理不能使ADX小鼠摆脱LT介导的死亡率。出人意料的是，口服DEX治疗还在所有测试剂量下均使肾上腺完整的DBA / 2J小鼠对LT致死性敏感，并且还加剧了BALB / cJ小鼠中LT介导的发病机制和死亡率。醛固酮不能保护ADX小鼠免受毒素攻击。这些结果表明，小鼠对炭疽病的敏感性取决于内分泌功能的良好平衡，但容易受到干扰。因此，在该疾病的治疗方案中必须考虑类固醇治疗炭疽的潜在有害后果。

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