Germaine G R, Tellefson L M
Infect Immun. 1982 Dec;38(3):1060-7. doi: 10.1128/iai.38.3.1060-1067.1982.
Glucose uptake was examined by using whole-cell suspensions of Streptococcus mutans (strains BHT, Ingbritt, and GS-5), Streptococcus mitis (strains 9811 and 72x41), and Actinomyces viscosus (strains T6 and WVU626) incubated for up to 90 min in 0 to 82% (vol/vol) human whole salivary supernatant. Glucose uptake by the S. mutans strains was completely inhibited at all saliva concentrations. Dithiothreitol (DTT), present during saliva incubation, prevented saliva inhibition. Glucose uptake was also restored when saliva-inhibited cells were subsequently exposed to DTT. The inclusion of catalase in the saliva incubation mixtures resulted in protection equal to that obtained with DTT. The S. mitis strains were also inhibited by saliva but to a far lesser extent that S. mutans. DTT and catalase also protected S. mitis from saliva inhibition. Both A. viscosus strains were completely refractory to saliva inhibition of glucose uptake. Based on (i) the sensitivity of the catalase-negative streptococci and the resistance of catalase-positive actinomyces to saliva inhibition and (ii) the equal and complete protection to saliva inhibition afforded by DTT and catalase, we conclude that the lactoperoxidase-SCN(-)-H(2)O(2) system in saliva was the only antibacterial system expressed under our experimental conditions. The relative resistance of S. mitis 9811 (compared with S. mutans BHT) to saliva inhibition was shown not to result from poor H(2)O(2) production in either glucose-supplemented buffer or saliva solutions. S. mitis produced inhibitory quantities of H(2)O(2) that equaled or exceeded S. mutans H(2)O(2) accumulation. It is suggested that S. mitis might possess a greater ability to repair lactoperoxidase-mediated damage than does S. mutans. Every organism studied exhibited a saliva concentration-dependent, cell growth-independent stimulation of glucose uptake after 60 to 90 min of incubation. The A. viscosus and S. mitis strains showed saliva stimulation (or stabilization) of glucose uptake with unsupplemented saliva. In the case of S. mutans, saliva stimulation was only observed when DTT was present. The possible role of salivary lactoperoxidase as a modulator of the intraoral site specificities exhibited by S. mutans is discussed.
利用变形链球菌（BHT菌株、Ingbritt菌株和GS - 5菌株）、缓症链球菌（9811菌株和72x41菌株）以及黏性放线菌（T6菌株和WVU626菌株）的全细胞悬液，在0至82%（体积/体积）的人全唾液上清液中孵育长达90分钟，检测葡萄糖摄取情况。在所有唾液浓度下，变形链球菌菌株的葡萄糖摄取均被完全抑制。唾液孵育期间存在的二硫苏糖醇（DTT）可防止唾液抑制作用。当唾液抑制的细胞随后暴露于DTT时，葡萄糖摄取也得以恢复。在唾液孵育混合物中加入过氧化氢酶可产生与DTT相同的保护作用。缓症链球菌菌株也受到唾液抑制，但程度远低于变形链球菌。DTT和过氧化氢酶也保护缓症链球菌免受唾液抑制。两种黏性放线菌菌株对唾液抑制葡萄糖摄取完全具有抗性。基于（i）过氧化氢酶阴性的链球菌对唾液抑制的敏感性以及过氧化氢酶阳性的放线菌对唾液抑制的抗性，以及（ii）DTT和过氧化氢酶对唾液抑制提供的同等且完全的保护作用，我们得出结论，唾液中的乳过氧化物酶 - SCN(-)-H₂O₂系统是在我们的实验条件下唯一表达的抗菌系统。已表明缓症链球菌9811（与变形链球菌BHT相比）对唾液抑制的相对抗性并非源于在补充葡萄糖的缓冲液或唾液溶液中过氧化氢产生不足。缓症链球菌产生的抑制量的过氧化氢等于或超过变形链球菌的过氧化氢积累量。提示缓症链球菌修复乳过氧化物酶介导损伤的能力可能比变形链球菌更强。每种研究的生物体在孵育60至90分钟后均表现出唾液浓度依赖性、与细胞生长无关的葡萄糖摄取刺激。黏性放线菌和缓症链球菌菌株在未补充唾液的情况下显示出唾液对葡萄糖摄取的刺激（或稳定）作用。就变形链球菌而言，则仅在存在DTT时观察到唾液刺激作用。讨论了唾液乳过氧化物酶作为变形链球菌所表现出的口腔内位点特异性调节剂的可能作用。
