Vogel S N, Moore R N, Sipe J D, Rosenstreich D L
J Immunol. 1980 Apr;124(4):2004-9.
C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.
C3H/HeJ小鼠在体内对细菌脂多糖（LPS）表现出明显的不敏感性。在给予LPS前11天用活卡介苗（BCG）微生物预处理这些小鼠，可使其对高度纯化的酚提取LPS的致死作用敏感。在卡介苗感染的C3H/HeJ小鼠中，其他对LPS的体内反应也随着致死率的提高而增加。这些反应包括：1）血清干扰素升高；2）急性期反应物血清淀粉样蛋白A（SAA）的产生；3）低血糖。然而，卡介苗感染对抗LPS抗体的产生影响极小。卡介苗感染的C3H/HeJ小鼠接近正常C3H/HeN小鼠的LPS敏感性，但增强的LPS敏感性是短暂的，在2个月内会降低。卡介苗在C3H/HeJ小鼠中诱导LPS敏感性的能力表明，LPS无反应性并非由于该品系存在绝对缺陷，而是一种部分可逆的低反应状态。此外，这些发现与其他观察结果表明，卡介苗感染诱导的LPS敏感性增强主要是通过对T细胞和/或巨噬细胞的作用介导的，而不是B淋巴细胞。
