Taichman N S, Hammond B F, Tsai C C, Baehni P C, McArthur W P
Infect Immun. 1978 Aug;21(2):594-604. doi: 10.1128/iai.21.2.594-604.1978.
Both virulent (V) and avirulent (AV) strains of Actinomyces viscosus T14 are capable of colonizing the oral cavity of gnotobiotic rats, but only T14-V causes destructive periodontal disease. The basis for this difference in in vivo pathogenicity has not been adequately defined. In the present study we compared the capacities of T14-AV and T14-V to provoke in vitro extracellular release of lysosomal constituents from human polymorphonuclear leukocytes (PMNs). In serum-free cultures, viable T14-V but not T14-AV stimulated discharge of PMN lysosomes. The release response was correlated with PMN phagocytic activity; thus, PMNs readily ingested T14-V but not T14-AV. To explain these differences in PMN-bacteria interactions, subcellular fractions of T14-AV or T14-V were incubated with PMNs. A crude, insoluble sonic extract derived from T14-V caused PMN lysosome release, but a similar fraction from T14-AV was inactive. However, following extensive washing and treatment with deoxyribonuclease or sodium dodecyl sulfate, cell wall fractions of T14-AV stimulated lysosome release. These procedures apparently removed an extracellular polysaccharide slime which is synthesized by T14-AV but not by T14-V. There was a significant reduction in the capacities of viable T14-V or cell wall fractions of T14-V or T14-AV to provoke PMN lysosome release when these agents were preincubated with a slime material isolated from T14-AV. This inhibitory influence of slime was overcome by the addition of fresh or heated (56 degrees C, 30 min) serum to the PMN-bacteria cultures. The data suggest a relationship between the abilities of the avirulent and virulent strains of A. viscosus T14 to act as periodontal pathogens in vivo and to serve as stimuli for PMN lysosome release in vitro.
黏性放线菌T14的强毒株(V)和无毒株(AV)都能够在悉生大鼠口腔中定殖,但只有T14-V会引发破坏性牙周病。这种体内致病性差异的基础尚未得到充分明确。在本研究中,我们比较了T14-AV和T14-V在体外刺激人多形核白细胞(PMN)溶酶体成分胞外释放的能力。在无血清培养中,活的T14-V而非T14-AV刺激了PMN溶酶体的释放。释放反应与PMN吞噬活性相关;因此,PMN很容易吞噬T14-V而不是T14-AV。为了解释PMN与细菌相互作用中的这些差异,将T14-AV或T14-V的亚细胞组分与PMN一起孵育。源自T14-V的粗制不溶性超声提取物会导致PMN溶酶体释放,但来自T14-AV的类似组分无活性。然而,经过大量洗涤并用脱氧核糖核酸酶或十二烷基硫酸钠处理后,T14-AV的细胞壁组分刺激了溶酶体释放。这些操作显然去除了一种由T14-AV而非T14-V合成的胞外多糖黏液。当这些制剂与从T14-AV分离的黏液物质预孵育时,活的T14-V或T14-V或T14-AV的细胞壁组分引发PMN溶酶体释放的能力显著降低。向PMN-细菌培养物中添加新鲜或加热(56℃,30分钟)的血清可克服黏液的这种抑制作用。数据表明黏性放线菌T14无毒株和强毒株在体内作为牙周病原体的能力与在体外作为PMN溶酶体释放刺激物的能力之间存在关联。