伴放线放线杆菌flp-1基因遗传多样性分析

目的:分析伴放线放线杆菌(Actinobacillus actinomycetemcomitans,Aa)临床分离菌株菌毛结构基因flp-1的遗传多样性和flp-1基因与菌株表型之间的关系.方法:对从不同牙周状况患者口腔中分离的60株Aa(57株粗糙型,3株传代转变成光滑型)和6株Aa标准菌株(光滑型)进行flp-1基因扩增,并通过PCR限制性片段长度多态性(PCR-RFLP)法分析临床分离菌株flp-1基因的遗传多样性.结果:所有57株粗糙型菌株和9株光滑型菌株都检测到flp-1基因;60株临床分离菌株检测到5种flp-1基因型,其中基因型2型占67%,共有40株.结论:Aa菌株表型的改变不伴有flp-1基因缺失;Aa临床分离菌株flp-1基因具有遗传多样性,基因型主要为2型.     

伴放线放线杆菌形态变化对菌体表面疏水性影响的研究

目的研究伴放线放线杆菌形态变化对菌体表面疏水性的影响。方法采用碳氢化合物法检测伴放线放线杆菌粗糙型和光滑型的菌体表面疏水性,观察同一菌株不同表型疏水性的变化。结果伴放线放线杆菌粗糙型和光滑型菌体表面具有疏水性。14株粗糙型伴放线放线杆菌菌体表面疏水率高于4株光滑型,差异有统计学意义（P〈0．05）。4株同源的粗糙型与其光滑型转变株比较得出除1株外,其余3株菌两种表型的菌体表面疏水率差异无统计学意义（P〉0．05）。结论伴放线放线杆菌形态变化可引起菌体表面疏水性的改变,粗糙型转变为光滑型后菌体表面疏水性减弱。     

伴放线放线杆菌形态变化对白细胞毒素分泌影响的研究

目的观察伴放线放线杆菌形态变化对白细胞毒素分泌的影响。方法选择粗糙型和光滑型伴放线放线杆菌各8株,应用聚丙烯酰胺凝胶电泳,检测液体培养12、24、48、60、72h的菌体及培养上清液中116kDa大小白细胞毒素蛋白条带的情况,应用超滤法分离纯化培养上清液蛋白,应用台盼蓝染色排除法检测上清液蛋白白细胞毒素活性。结果粗糙型伴放线放线杆菌菌株液体培养12、24、48、60、72h菌体蛋白电泳均可见116kDa大小的蛋白条带,培养上清液蛋白电泳结果显示116kDa大小的蛋白条带均出现于培养24和48h;光滑型伴放线放线杆菌菌株液体培养12、24、48、60、72h菌体蛋白电泳结果均缺少116kDa大小的蛋白条带,培养上清液蛋白电泳结果显示116kDa大小的蛋白条带出现于培养12和24h;实验菌株培养上清液提取蛋白均具有白细胞毒素活性。结论伴放线放线杆菌粗糙型和光滑型菌株均可分泌具有直接杀灭人多形核白细胞活性的白细胞毒素,但粗糙型菌株分泌白细胞毒素的时间晚于光滑型。     

伴放线放线杆菌光滑株与粗糙株生长及磷酸胆碱表达的比较研究

目的 绘制伴放线放线杆菌同一菌株不同表型的生长曲线,测定菌体蛋白表达上的差异。方法 采用液体培养基TSB培养伴放线放线杆菌分离株D7S及其光滑型菌株D7SS,紫外分光光度计检测细菌密度,连续观测30h,绘制生长曲线。聚丙烯酰胺凝胶(SDS-PAGE)电泳后考马斯亮蓝染色比较两种表型的细菌蛋白的差异。免疫印迹法(Western Blot)观察两种表型细菌蛋白对单克隆抗体TEPC-15的反应情况。结果 D7SS菌株比D7S菌株更早进入对数期和衰亡期;两型细菌全细胞蛋白电泳考马斯亮蓝染色时蛋白带未见明显差异;免疫印迹分析D7S菌株在分子质量接近10ku的蛋白中存在磷酸胆碱,而D7SS中未发现。结论 伴放线放线杆菌D7S和其光滑型菌株D7SS的生长曲线以及对TEPC-15抗体的反应性明显不同。     

伴放线放线杆菌血清型分析

目的 PCR法检测伴放线放线杆菌（Actinobacillus actinomy＇etemcomitans，Aa）临床分离菌株血清型，分析其与flp-1基因型的关系。方法用血清型特异性引物，通过普通PCR和多重PCR的方法对60株Aa临床分离菌株的血清型进行鉴定，并分析其与flp-1基因型的关系。结果 60株Aa临床分离菌株中血清型c型63，33％，e型23．33％，b型6.67％，a，f型各占3．33％，未检测到d型菌株；在24名被检测者中，15名检测到c型An菌株，3名检测到b型菌株，各有2名分别检测到a、e、f型菌株。fip-1基因型Ⅰ型菌株的血清型均为a型，40株Ⅱ型菌株中38株为c型，Ⅳ型菌株均为b型，11株Ⅴ型菌株中9株为e型，Ⅵ型菌株均为e型。结论 Aa血清型分布以c型为主，fip-1基因型与菌株血清型存在一定对应关系。     

伴放线放线杆菌血液感染菌株的血清型分析

目的探讨不同血清型伴放线放线杆菌在全身血液感染中的分布规律。方法采用聚合酶链反应（polymerase chain reaction,PCR）方法对29株从全身感染患者血液中分离培养的伴放线放线杆菌菌株进行血清型分析,采用ATCC 29523（血清型a）、ATCC 43718（血清型b）、ATCC 33384（血清型c）、IDH781（血清型d）、IDH1705（血清型e）以及CU1000（血清型f）作为伴放线放线杆菌参考菌株。根据伴放线放线杆菌不同血清型特异性多糖抗原基因序列设计6对不同的寡核苷酸引物,用这6对引物分别对上述菌株的DNA进行PCR扩增分析。结果每一对引物均针对相应血清型的参考菌株产生特异性单一条带PCR产物,血清型a、b、c、d、e、f菌株的PCR产物大小分别为428、298、559、690、211、232bp。29株血源性临床分离菌株中血清型b16株（55%）,血清型a和c各4株（14%）,血清型d和f各2株（7%）,还有1株无法鉴定为上述任何一种血清型。结论血液中分离培养的伴放线放线杆菌以血清型b为主,其次是血清型a和c。     

放线共生放线杆菌显微形态学的研究

目的 观察放线共生放线杆菌不同菌落菌株形态特点，探讨其致病的形态学基础。方法 粗糙型和光滑型两种菌落形态的细菌固体培养2天-4天应用电子显微镜阴性染色的方法比较观察放线共生放线杆菌菌体表面结构特点。结果 粗糙型菌落菌体菌毛丰富；刚刚转变后的光滑型菌落菌体仍可存在菌毛，但这种菌落继续传代菌毛可完全失去，菌毛表现为几种形态，细密或稀疏，也可成束状或网状，粗糙型菌体染色深，不均匀，菌体边缘不规则，视野不干净，多次传代后的光滑型菌落，菌体染色浅且均匀，菌体饱满透明，视野干净，粗糙型可以见到膜泡样的结构，但量很少。结论 粗糙型和光滑型菌的菌体形态存在明显的差异。主要表现为菌毛。     

伴放线放线杆菌菌落生长形态变化的观察

目的：观察伴放线放线杆菌（Actinobacillus actinomycetemcomitans,Aa)从粗糙型到光滑型的转变过程，认别Aa在实验室传代过程中出现的不同生长形态。方法：从牙周炎患者龈下菌班中分离出的原代菌株8株，应用固体及液体培养基连续传代，液体培养每次传代的同时接种固体培养基观察相应的菌落形态。结果：液体培养获得3株光滑型转变株。菌落的变化从粘附的小菌落到沉淀的大菌落到完全的均匀生长，转化过程大约需要7－8代。在这一过程中相应传至固体培养基上生长的Aa从粘附的半透明的小菌落变大、不透明并失去粘附的特性，又随着边缘的扩散变为扁平，透明度也增加；与此同进内部的星形结构逐渐变简单、变小，最后消失。固体培养未获得典型的转变株。结论：Aa从粗糙型到光滑型的转变是一个菌落湿度逐渐增加，体积逐渐增大，并逐渐失去内部结构的过程。这一过程至少可以看到半透明突起的粗糙型，不透明突起的光滑型和近乎透明的扁平光滑型3种菌落形态。     

采用PCR方法鉴别伴放线放线杆菌的6种血清型

目的：探索采用PCR的方法对伴放线放线杆菌的不同菌株进行血清型分类。方法：根据伴放线放线杆菌不同血清型特异性多糖抗原基因序列设计6对不同的寡核苷酸引物，用这6对引物分别对所选择伴放线放线杆菌6种不同的血清型菌株各3株，共18株，其中参考菌株6株，系ATCC29523（血清型a），ATCC43718（血清型b），ATCC33384（血清型c），IDH781（血清型d），IDH1705（血清型e）以及CU1000（血清型f），其余12个菌株均为临床分离株的DNA进行PCR扩增分析。结果：每一对引物均针对相应的血清型产生特异性单一条带PCR产物，产物大小分别为428bp（a），298bp（b），559bp（c），690bp（d），211bp（e），232bp（f）。全部18个菌株均能够被准确识别，无交叉反应。结论：PCR方法可以快速准确地鉴别伴放线放线杆菌目前已知的全部6种血清型。     

放线共生放线杆菌白细胞毒素水平检测

目的　检测放线共生放线杆菌 (Actinobacillusactinomycetemcomitans,Aa)临床分离菌株白细胞毒素水平 ,区分高毒株与低毒株。方法　应用聚合酶链反应 (polymerasechainreaction ,PCR)检测白细胞毒素操纵子启动子区域基因序列的差异。检测临床菌株 6 8株 ,其中b型 17株 ,c型 42株 ,a型9株。阳性对照高毒株为JP2 ,低毒株为ATCC43717等 5株Aa国际参考菌株 ,阴性对照为 12株异种菌国际参考菌株。结果　 6 8株临床分离菌株扩增片段均为 10 2 2bp ,JP2扩增片段为 492bp ,ATCC43717等 5株扩增片段均为 10 2 2bp ,12株异种菌参考菌株无扩增片段出现。结论　 6 8株临床分离菌株全部为低毒株     

Sequence diversity in the major fimbrial subunit gene (flp-1) of Actinobacillus actinomycetemcomitans

Cells of the periodontal pathogen Actinobacillus actinomycetemcomitans exhibit tight adherence to surfaces such as glass, plastic and hydroxyapatite, a property that probably plays an important role in the ability of this bacterium to colonize teeth and other surfaces. Tight adherence is mediated by long fibrils of bundled pili (fimbriae) that form on the surface of the cell. The flp-1 gene encodes the major pilin protein component of A. actinomycetemcomitans fimbriae. In this study we compared flp-1 DNA sequences from 43 strains of A. actinomycetemcomitans isolated in Europe, Japan and the United States and identified seven distinct flp-1 allelic classes. DNA and predicted protein sequences were almost completely conserved within each flp-1 class but were highly divergent between classes. Most amino acid substitutions occurred in the C-terminus of the pilin protein, a region that has been shown to be important for the bundling and adhesive properties of the pili. flp-1 classes correlated with serotypes and 16S rRNA genotypes in most strains. At least five strains showed evidence of horizontal transfer of flp-1 between strains of different serotypes and 16S rRNA genotypes. Four of the seven flp-1 classes were present in geographically diverse isolates. Strains representing all seven flp-1 classes, but not a strain carrying a transposon insertion in flp-1, bound avidly to polystyrene in an in vitro adherence assay. Strains representing six of the seven flp-1 classes were isolated from localized juvenile periodontitis patients, suggesting that phylogenetically diverse strains carry pathogenic potential. Our findings provide a framework for future biochemical, immunological and genetic studies of A. actinomycetemcomitans fimbriae.     

Adhesion and invasion to epithelial cells by fimA genotypes of Porphyromonas gingivalis

Adhesion to and invasion of epithelial cells by the periodontopathogen Porphyromonas gingivalis is promoted by the major fimbriae, encoded by fimA. The microorganism can be classified in six genotypes, based on fimA sequence, and genotype II strains are more prevalent than others in periodontitis patients. This study aimed to determine the adhesive and invasive abilities on KB cells of different fimA allelic variants of P. gingivalis isolates. Twenty-two isolates and six reference strains representing the six fimA genotypes and non-typeable strains were screened for their adhesion and invasion abilities on KB cells, using standard methods. All strains were able to adhere and, except for one, to invade KB cells. However, these properties were not homogeneous among strains belonging to the same genotype. There was no correlation between adhesion and invasion efficiencies. Isolate KdII 865 (fimA genotype II) was the most invasive and the second most adhesive strain, whereas reference strain ATCC 33277 (fimA I) showed a low adhesion ability but was highly invasive. These data indicated that fimA genotypes of P. gingivalis are not related to the adhesion and invasion abilities on KB cells, suggesting that the increased prevalence and proportion of certain genotypes may be attributed to other characteristics besides FimA variation.     

Quantitative analysis of the adhesion of cariogenic streptococci to orthodontic metal brackets

The aim of this study was to analyze the adhesion of cariogenic streptococci to orthodontic metal brackets in terms of the type of bacterial strains, the incubation time, and saliva coating. Two strains of Streptococcus mutans (S. mutans LM7 and S. mutans OMZ65) and two strains of S. sobrinus (S. sobrinus B13 and S. sobrinus 6715) were used. Twenty metal brackets were incubated with either unstimulated whole saliva or phosphate-buffered saline for two hours. The bacterial adhesion assays were then performed by incubating the tritium-labeled streptococci with saliva-coated or noncoated orthodontic brackets for three, six, or nine hours. The results showed a characteristic binding pattern according to the type of bacterial strains used. S. mutans OMZ65 showed the highest amount of adhesion, whereas S. sobrinus B13 showed the lowest amount of adhesion. Generally, an extended incubation time increased the adhesion of cariogenic streptococci, and the amount of adhesion was the highest after nine hours of incubation. The saliva coating did not significantly influence the adhesion of bacteria. However, this saliva-mediated adhesion differed according to incubation time. The saliva coating tended to gradually decrease the adhesion by the extended incubation time, compared with the noncoated controls. This study indicates that each strain of cariogenic streptococci has a characteristic adhesion pattern and the type of bacterial strain, the incubation time, and saliva influenced the adhesion.     

不同孵育时间具核梭杆菌黏附和侵入上皮细胞的变化

目的：观察在具核梭杆菌（F.nucleatum，Fn）黏附和侵入上皮细胞的早期阶段，不同时间黏附量和侵入量的变化以及砌不同菌株之间黏附和侵入能力的差别。方法：将实验菌Fn ATCC10953以及Fn WCD05-1分别配成菌悬液，加入培养有上皮细胞（KB）的24孔细胞培养板中。孵育0．5、1、2、3、4h进行黏附和侵入测定。初步探索时间与砌黏附和侵入KB细胞的数量之间是否存在相关关系。结果：在黏附和侵入早期，随相互作用时间延长，砌黏附和侵入KB细胞的数量增加，并且临床株的黏附和侵入能力明显优于标准株。在达到最大黏附和侵入量以后，细菌量有一定下降，但是至少在短时间内可以保持一定的黏附和侵入水平。达到黏附和侵入的最大值时，临床株的黏附和侵入量分别约是标准株的2倍和4倍。结论：在黏附和侵入早期，随相互作用时间延长，砌黏附和侵入KB细胞的数量增加，并且临床株WCD05-1显示出比标准株ATCC10953更强的黏附和侵入能力。达到最大值后其黏附和侵入量有一定下降。     

The influence of morphological variation on Candida albicans adhesion to denture acrylic in vitro.

Using denture acrylic pieces coated with either whole human stimulated saliva or oral streptococci, the binding ability of three different Candida albicans strains was investigated. The C. albicans strains include a clinical isolate with the commonly observed, smooth, round colonial morphology (strain 613p), a morphological variant spontaneously derived from the clinical isolate strain 613p (strain 613m1BK) and a clinical isolate from an oral lesion that was also a morphological variant upon primary isolation (strain 228). Levels of adhesion to the acrylic pieces were determined radiometrically using C. albicans cells metabolically labelled with [35S]-methionine. Whole stimulated saliva significantly increased the binding of all strains compared to uncoated acrylic. However, the level of binding of strain 613p to saliva-coated acrylic was significantly greater than the levels observed for the morphological variant strain 613m1BK. Coating acrylic pieces with either Streptococcus sanguis NCTC 10904, Strep. mutans GS-5 or Strep. sobrinus ATCC 27352 instead of saliva resulted in significantly greater binding by strain 613p compared to uncoated acrylic. Pre-coating the acrylic with the oral streptococci did not significantly increase the binding of morphological variant strains 613m1BK and 228 compared to uncoated acrylic. In general, preincubation of adherent streptococci with sucrose to induce the synthesis of extracellular carbohydrate polymers did not significantly increase the binding levels of the C. albicans strains above those observed using streptococci in buffer alone. Compared to its parental strain 613p, morphological variant strain 613m1BK adhered poorly to denture acrylic coated with either salivary constituents or oral streptococci, while strain 228 adhered to the same substrates at an intermediate level. Furthermore, physical disaggregation of clusters of the morphological variant strain 613m1BK did not appear to increase its binding capacity to saliva-coated denture acrylic. The effect of whole stimulated saliva on the adherence of C. albicans 613p to a variety of plastic substrates in addition to denture acrylic was examined. Overall, saliva pre-coating of the various plastics promoted C. albicans 613p adhesion. The adhesion of strain 613p to denture acrylic coated with whole stimulated saliva from each of five different donors or with parotid and submandibular/sublingual saliva from each of two donors was also examined. Regardless of donor, a coating of whole stimulated saliva significantly increased the binding of strain 613p to denture acrylic compared to uncoated acrylic. In addition, a coating of parotid saliva significantly increased the binding of strain 613p to denture acrylic compared to submandibular/sublingual saliva.     

Adhesion of Candida albicans, but not Candida krusei, to salivary statherin and mimicking host molecules

The aim of the present study was to identify salivary molecules affecting adhesion of Candida albicans and Candida krusei to salivary pellicles and epithelial cells. Strains of C. albicans (GDH18, GDH3339, CA1957, ATCC 28366 and ATCC 10321), but not C. krusei (strains ATCC 14243 and Ck9), bound to saliva-coated hydroxyapatite and buccal epithelial cells. Parotid saliva fractions containing statherin, glycosylated proline-rich proteins (PRP) and as yet unidentified components mediated adhesion of strain GDH18; Fuc alpha 1-2Gal beta 1-4Glc partly inhibited the adhesion to those fractions not containing statherin. Pure statherin, but not PRP-1, mediated dose-dependent adhesion of C. albicans strain GDH18 to hydroxyapatite beads. Candida isolates (GDH18, GDH3339 and CA1957) bound somewhat more avidly to statherin/saliva relative to ATCC strains 28366 and 10321, while the opposite was true for adhesion to buccal epithelial cells. Adhesion of C. albicans strain GDH18 to saliva-coated hydroxyapatite and buccal epithelial cells was completely (93%) and partly (43%) blocked by statherin-specific immunoglobulin G (IgG) antibodies, respectively. Control IgG antibodies did not block Candida adhesion. Blockage of Candida adhesion to epithelial cells also occurred with Fuc alpha 1-2Gal beta 1-4Glc (49%) and N-acetylglucosamine (38%), while statherin specific IgG antibodies in combination with Fuc alpha 1-2Gal beta 1-4Glc almost completely eliminated Candida adhesion (79%). In addition, statherin in solution blocked the adhesion of strain GDH18 to epithelial cells by inducing aggregation of Candida cells.     

Sucrose-dependent accumulation of oral streptococci and their adhesion-defective mutants on saliva-coated hydroxyapatite

The adhesion and accumulation of oral streptococci on saliva-coated hydroxyapatite was examined in strains representing species that appear in initial plaque ( Streptococcus sanguise FC1 and Streptococcus oralis C5) and in more mature plaque ( Streptococcus gordonii G9B). Washed cells of strains FC1 and C5 did not attach better to saliva-coated hydroxyapatite than did strain G9B, suggesting that the degree of initial adhesiveness does not alone account for the temporal appearance of these bacteria in dental plaque. Growing cells of each strain were also examined for their ability to accumulate on saliva-coated hydroxyapatite. The addition of sucrose to the medium promoted the accumulation of strain G9B more than it promoted the accumulation of strains FC1 and C5. Sucrose also enhanced the accumulation of adhesion-defective mutants of each strain to levels similar to those of the respective parent strains. These results suggest that sucrose-dependent accumulation may facilitate the colonization of the tooth surface by these species of oral streptococci when adhesion is limited by reduced bacterial adhesiveness or limited pellicle-binding sites.     

Quantitative determination of adhesion patterns of cariogenic streptococci to various orthodontic adhesives

OBJECTIVE: To investigate the adhesion of various cariogenic streptococci to orthodontic adhesives. MATERIALS AND METHODS: Five light-cure orthodontic adhesives (one fluoride-releasing composite, three non-fluoride-releasing composites, and one resin-modified glass ionomer cement) were used. The adhesive type, bacterial strain, incubation time, and saliva coating were studied. Thirty specimens of each adhesive were incubated with unstimulated whole saliva or phosphate-buffered saline for 2 hours. Binding assays were then performed by incubating tritium-labeled streptococci with the adhesives for 3 or 6 hours. RESULTS: The results showed a characteristic adhesion pattern according to the type of bacterial strains used. Streptococcus mutans LM7 showed the highest amount of adhesion, whereas S sobrinus B13 showed the lowest amount of adhesion. The cariogenic streptococci adhered to the glass ionomer significantly more than to the composites, whereas there was no significant difference in the adhesion amount among the four composites. The extended incubation time significantly increased bacterial adhesion. However, saliva coating did not significantly alter adhesion patterns of cariogenic streptococci. CONCLUSIONS: This study suggests that cariogenic streptococci can adhere diversely according to adhesive type and that the adhesion of the cariogenic streptococci is not influenced by its fluoride-releasing properties.     

Adhesion of Candida albicans,but not Candida krusei,to salivary statherin and mimicking host molecules

The aim of the present study was to identify salivary molecules affecting adhesion of Candida albicans and Candida krusei to salivary pellicles and epithelial cells. Strains of C. albicans (GDH18, GDH3339, CA1957, ATCC 28366 and ATCC 10321), but not C. krusei (strains ATCC 14243 and Ck9), bound to saliva‐coated hydroxyapatite and buccal epithelial cells. Parotid saliva fractions containing statherin, glycosylated proline‐rich proteins (PRP) and as yet unidentified components mediated adhesion of strain GDH18; Fucα1‐2Galβ1‐4Glc partly inhibited the adhesion to those fractions not containing statherin. Pure statherin, but not PRP‐1, mediated dose‐dependent adhesion of C. albicans strain GDH18 to hydroxyapatite beads. Candida isolates (GDH18, GDH3339 and CA1957) bound somewhat more avidly to statherin/saliva relative to ATCC strains 28366 and 10321, while the opposite was true for adhesion to buccal epithelial cells. Adhesion of C. albicans strain GDH18 to saliva‐coated hydroxyapatite and buccal epithelial cells was completely (93%) and partly (43%) blocked by statherin‐specific immunoglobulin G (IgG) antibodies, respectively. Control IgG antibodies did not block Candida adhesion. Blockage of Candida adhesion to epithelial cells also occurred with Fucα1‐2Galβ1‐4Glc (49%) and N‐acetylglucosamine (38%), while statherin specific IgG antibodies in combination with Fucα1‐2Galβ1‐4Glc almost completely eliminated Candida adhesion (79%). In addition, statherin in solution blocked the adhesion of strain GDH18 to epithelial cells by inducing aggregation of Candida cells.     

Prevotella intermedia ATCC 25611 targets host cell lamellipodia in epithelial cell adhesion and invasion

Introduction:  The Prevotella intermedia group bacteria, namely P. intermedia , Prevotella nigrescens , and Prevotella pallens , are phylogenetically closely related and potentially connected with oral and gastrointestinal tract disease pathogenesis. The aim of the present study was to examine whether these species differ in their capabilities of adhesion to and invasion of epithelial cells.
Methods:  Adhesion and invasion were assayed by standard antibiotic/culture assays and fluorescent microscopy techniques. The effect of Prevotella strains on epithelial cell viability was measured using a commercial cell proliferation assay.
Results:  The strains P. intermedia ATCC 25611 and P. nigrescens ATCC 33263 adhered to epithelial cells, the adhesion numbers of P. intermedia being twice as high as those of P. nigrescens . These strains invaded epithelial cells but invasion was weak. The adhesion of P. intermedia was specifically targeted to epithelial cell lamellipodia. The number of adhered P. intermedia cells increased or decreased when the formation of lamellipodia was stimulated or inhibited, respectively. None of the tested strains showed toxic effects on epithelial cells; a clinical P. intermedia strain even increased the number of viable cells by about 20%.
Conclusion:  The results suggest that among the P. intermedia group bacteria, P. intermedia and P. nigrescens type strains can adhere to and invade epithelial cells, the capability of P. intermedia ATCC 25611^T being highest in this context. This strain proved to have a special affinity in binding to epithelial cell lamellipodia.