Comparative virulence of periodontopathogens in a mouse abscess model.
Comparative virulence of periodontopathogens in a mouse abscess model.
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DOI：
10.1111/j.1601-0825.1995.tb00174.x
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发表时间：
2008-06
期刊：
影响因子：
3.8
通讯作者：
J. Ebersole;L. Kesavalu;S. Schneider;R. Machen;S. Holt
中科院分区：
文献类型：
--
作者：
J. Ebersole;L. Kesavalu;S. Schneider;R. Machen;S. Holt
目的（S）本报告比较了选定的牙龈卟啉单胞菌、A。actinomycetemcomitans、伴放线菌C. rectus、F. nucleatum和T.在小鼠模型中检测齿垢作为这些口腔微生物的致病潜力的量度。与这些单一感染相关的组织破坏的特征与细菌协同作用在进行性牙周炎中的潜在模型相关。设计和方法所有细菌菌株生长至对数中期至早期稳定生长期，收获并以各种剂量用于攻击BALB/c正常小鼠和BALB/c地塞米松（DEX）处理的小鼠以模拟中性粒细胞功能障碍。作为挑战剂量和时间的函数，检查了这些物种的组织破坏特征和明显的组织破坏能力。结果测量在攻击后约15天的时间间隔内检查小鼠，并评估病变的存在/不存在、病变的局部或全身性质（包括以mm 2为单位的大小）和感染的致死率。结果与致死率和与结缔组织破坏相关的病变大小相关的各种牙龈卟啉单胞菌菌株的毒力的比较表明牙龈卟啉单胞菌菌株53977>W50 = T22>3079>33277>381的毒力能力。C.腹直肌引起局限于皮肤上皮层的局部坏死损伤。病变的大小也表明了毒性的分级差异，例如C。直肌菌株234>576>> 33238。A.伴放线菌引起典型的局部脓肿形成，伴有中性粒细胞浸润和炎性渗出物。虽然A.放线菌共生菌株在该小鼠模型中表现出相似的毒力模式，A.伴放线菌血清型B代表菌株的致病力较强，毒力大小为3113 D-N = 3975 A> JP 2> or = Y 4>29523>33384。两个C. rectus和A.放线菌共生菌株显示出明确的证据，最近的临床分离株比实验室菌株更毒力。挑战F。nucleatum导致组织破坏性反应，这与本研究中使用的其他菌株所观察到的不同。在F.核质在低F时，组织受累也更大。与其他细菌相比，核质剂量。F. DEX处理的小鼠的核质攻击导致向开放性损伤的转变。T.在这项研究中，齿垢似乎比其他物种更具组织侵入性。用T.齿垢导致包括上皮和结缔组织在内的多种组织受累，并且似乎侵入肌肉层和更深的组织。除了侵入更深的组织外，由此产生的病变需要相当长的时间才能解决。在DEX处理的小鼠（中性粒细胞耗尽）中，牙龈卟啉单胞菌、C. rectus和A.放线菌共生菌的毒力明显更强。相反，DEX治疗改变了F. nucleatum，F. nucleatum和T.齿垢没有明显增强。结论：本研究的结果表明，不同的微生物有能力提供个别的病理可能会在一个添加剂/协同作用的方式有助于牙周炎中注意到的组织破坏。
OBJECTIVE(S) This report compares the virulence of selected strains of P. gingivalis, A. actinomycetemcomitans, C. rectus, F. nucleatum and T. denticola in a murine model as a measure of pathogenic potential of these oral microorganisms. The characteristics of the tissue destruction associated with these monoinfections were then related to a potential model for bacterial synergism in progressing periodontitis. DESIGN AND METHODS All bacterial strains were grown to mid-logarithmic to early stationary growth phase, harvested and used at various doses to challenge BALB/c normal and BALB/c dexamethasone (DEX) treated mice to mimic a neutrophil dysfunction. The characteristics of tissue destruction, and overt tissue destructive capacity of these species were examined as a function of challenge dose and time. OUTCOME MEASURES The mice were examined for an interval of approximately 15 days post-challenge and the presence/absence of lesions, localized or generalized nature of the lesion (including size in mm2), and lethality of the infection were assessed. RESULTS Comparison of the virulence of the various P. gingivalis strains related to lethality and lesion size associated with destruction of the connective tissue, indicated a virulence capacity of P. gingivalis strains 53977>W50 = T22>3079>33277>381. C. rectus elicited localized necrotic lesions which were limited to the epithelial layers of the skin. The size of the lesions also indicated a graded difference in virulence, such that C. rectus strains 234>576>>33238. A. actinomycetemcomitans caused the formation of classic localized abscesses with a PMN infiltrate and inflammatory exudates. Although each of the A. actinomycetemcomitans strains exhibited a similar virulence pattern in this murine model, A. actinomycetemcomitans serotype b representative strains were potentially more pathogenic with a virulence capacity of 3113D-N = 3975A>JP2 > or = Y4>29523>33384. Both C. rectus and A. actinomycetemcomitans strains showed clear evidence that recent clinical isolates were more virulent than laboratory strains. Challenge with F. nucleatum resulted in tissue destructive responses which were different from those observed with the other strains used in this study. A rapid onset of dose-dependent lesion development, related to the formation of either closed abscesses or open lesions, was observed with F. nucleatum. Tissue involvement was also greater at lower F. nucleatum doses when compared to the other bacteria. F. nucleatum challenge of DEX-treated mice resulted in a shift to open lesions. T. denticola appeared to be more tissue invasive than the other species examined in this study. Challenge of mice with T. denticola resulted in involvement of multiple tissues, including epithelial and connective tissues, as well as appearing to invade muscle layers and deeper tissues. In addition to invading deeper tissues, the resulting lesions took considerably longer to resolve. In the DEX-treated mice (neutrophil depleted), P. gingivalis, C. rectus, and A. actinomycetemcomitans were significantly more virulent. In contrast, while DEX treatment altered the characteristics of lesions caused by F. nucleatum, the extent of lesions produced by F. nucleatum and T. denticola was not substantially enhanced. CONCLUSIONS The results obtained from this study suggest that different microorganisms have the ability to provide individual pathologies which may act in an additive/synergistic fashion contributing to the tissue destruction noted in periodontitis.