Hammond B F, Lillard S E, Stevens R H
Infect Immun. 1987 Mar;55(3):686-91. doi: 10.1128/iai.55.3.686-691.1987.
An inhibitory factor from Actinobacillus actinomycetemcomitans Y4 was isolated, and its properties indicated that it was a bacteriocin (actinobacillicin). The bacteriocin was active against Streptococcus sanguis strains, Streptococcus uberis (FDC1), and Actinomyces viscosus T14 as well as other strains of A. actinomycetemcomitans, but not against other crevicular bacteria, including other streptococci and actinomycetes. The activity of this bacteriocin was inhibited by pronase, trypsin, and heat (45 min at 56 degrees C) but not by DNase, RNase, phospholipase, exposure to UV light, or low pH (1.0 to 6.5). Although actinobacillicin markedly inhibited glycolysis in S. sanguis, the primary mechanism of its bactericidal action appears to be alterations in cell permeability, with the resultant leakage of RNA, DNA, and other essential intracellular macromolecules. These findings provide an ecologic explanation for the reciprocal growth relationship between A. actinomycetemcomitans and S. sanguis/Actinomyces viscosus observed in localized juvenile periodontitis.
从伴放线放线杆菌Y4中分离出一种抑制因子，其特性表明它是一种细菌素（放线杆菌素）。该细菌素对血链球菌菌株、乳房链球菌（FDC1）、粘性放线菌T14以及其他伴放线放线杆菌菌株具有活性，但对其他龈沟细菌无活性，包括其他链球菌和放线菌。该细菌素的活性被链霉蛋白酶、胰蛋白酶和热（56℃ 45分钟）抑制，但不被DNA酶、RNA酶、磷脂酶、紫外线照射或低pH值（1.0至6.5）抑制。虽然放线杆菌素显著抑制血链球菌的糖酵解，但其杀菌作用的主要机制似乎是细胞通透性的改变，导致RNA、DNA和其他必需的细胞内大分子泄漏。这些发现为局限性青少年牙周炎中观察到的伴放线放线杆菌与血链球菌/粘性放线菌之间的相互生长关系提供了生态学解释。
