O'Brien A D, McClung H J, Kapral F A
Infect Immun. 1978 Jul;21(1):102-13. doi: 10.1128/iai.21.1.102-113.1978.
Prior studies had shown that Staphylococcus aureus delta-toxin was able to inhibit water absorption in guinea pig ileum and to elevate the cyclic AMP content of this tissue, but was unable to elicit certain cyclic AMP-mediated changes in Y-1 adrenal or Chinese hamster ovary cells. Because water movement passively follows the net movement of electrolytes in the gut, this study investigated the effect of delta-toxin on ion transport in guinea pig ileum maintained in vitro. The transmural potential difference (PD) of guinea pig ileum was measured and nullified with an automatic voltage clamp. The short circuit flowing under these conditions (I(sc)) was measured, and the conductance was calculated (I(sc)/PD). Unidirectional (22)Na(+) and (36)Cl(-) fluxes were measured. In a glucose-free Ringer solution, delta-toxin caused an immediate spike in PD and I(sc), and the extent and duration of the spike generally increased with increasing toxin concentration. The conductance of ileum was increased by delta-toxin, and this effect on conductance could be blocked by lecithin, a known inhibitor of delta-toxin. Tissue in the presence of glucose did not exhibit a spike in PD or I(sc) when exposed to delta-toxin. In a glucose-free medium, delta-toxin caused a 1.5- to 2.5-fold increase in both the unidirectional absorption and secretion of Na(+) and Cl(-), whereas the net secretion of Na(+) increased above basal levels. The observation that delta-toxin causes a prompt increase in intestinal ion flux lends credence to the concept that the elevation in cellular cyclic AMP, which occurs later, is a secondary response to the toxin. The rapid increase in ion flux may reflect the ability of delta-toxin to augment intercellular movement of ions across the mucosa rather than the stimulation of transcellular processes.
先前的研究表明，金黄色葡萄球菌δ-毒素能够抑制豚鼠回肠对水的吸收，并提高该组织中环磷酸腺苷（cAMP）的含量，但无法在Y-1肾上腺细胞或中国仓鼠卵巢细胞中引发某些由cAMP介导的变化。由于肠道中的水被动地跟随电解质的净移动，本研究调查了δ-毒素对体外培养的豚鼠回肠离子转运的影响。测量豚鼠回肠的跨膜电位差（PD），并用自动电压钳使其归零。测量在这些条件下的短路电流（I(sc)），并计算电导（I(sc)/PD）。测量单向（22）Na(+)和（36）Cl(-)通量。在无葡萄糖的林格氏溶液中，δ-毒素导致PD和I(sc)立即出现峰值，并且峰值的程度和持续时间通常随着毒素浓度的增加而增加。δ-毒素增加了回肠的电导，这种对电导的影响可以被卵磷脂（一种已知的δ-毒素抑制剂）阻断。当暴露于δ-毒素时，存在葡萄糖的组织在PD或I(sc)中未表现出峰值。在无葡萄糖的培养基中，δ-毒素导致Na(+)和Cl(-)的单向吸收和分泌增加1.5至2.5倍，而Na(+)的净分泌增加到基础水平以上。δ-毒素导致肠道离子通量迅速增加这一观察结果支持了这样的概念，即稍后发生的细胞内cAMP升高是对毒素的继发性反应。离子通量的快速增加可能反映了δ-毒素增强离子跨粘膜细胞间移动的能力，而不是刺激跨细胞过程的能力。
