Pron B, Boumaila C, Jaubert F, Sarnacki S, Monnet J P, Berche P, Gaillard J L
Laboratoire de Microbiologie, Institut National de la Santé et de la Recherche Médicale U411, Faculté de Médecine Necker-Enfants Malades, Paris, France.
Infect Immun. 1998 Feb;66(2):747-55. doi: 10.1128/IAI.66.2.747-755.1998.
The intestinal stage of listeriosis was studied in a rat ligated ileal loop system. Listeria monocytogenes translocated to deep organs with similar efficiencies after inoculation of loops with or without Peyer's patches. Bacterial seeding of deep organs was demonstrated as early as 15 min after inoculation. It was dose dependent and nonspecific, as the delta inlAB, the delta hly, and the delta actA L. monocytogenes mutants and the nonpathogenic species, Listeria innocua, translocated similarly to wild-type L. monocytogenes strains. The levels of uptake of listeriae by Peyer's patches and villous intestine were similar and low, 50 to 250 CFU per cm2 of tissue. No listeria cells crossing the epithelial sheet of Peyer's patches and villous intestine were observed by transmission electron microscopy. The lack of significant interaction of listeriae and the follicle-associated epithelium of Peyer's patches was confirmed by scanning electron microscopy. The follicular tissue of Peyer's patches was a preferential site of Listeria replication. With all doses tested, the rate of bacterial growth was 10 to 20 times higher in Peyer's patches than in villous intestine. At early stages of Peyer's patch infection, listeriae were observed inside mononuclear cells of the dome area. Listeriae then disseminated throughout the follicular tissue except for the germinal center. The virulence determinants hly and, to a lesser extent, actA, but not inlAB, were required for the completion of this process. This study suggests that Peyer's patches are preferential sites for replication rather than for entry of L. monocytogenes, due to the presence of highly permissive mononuclear cells whose nature remains to be defined.
利用大鼠结扎回肠袢系统对李斯特菌病的肠道阶段进行了研究。在接种有或没有派尔集合淋巴结的肠袢后，单核细胞增生李斯特菌以相似的效率转移至深部器官。接种后15分钟就证实了深部器官中有细菌定植。这是剂量依赖性且非特异性的，因为单核细胞增生李斯特菌的ΔinlAB、Δhly和ΔactA突变体以及非致病菌种无害李斯特菌与野生型单核细胞增生李斯特菌菌株的转移情况相似。派尔集合淋巴结和绒毛状肠对李斯特菌的摄取水平相似且较低，每平方厘米组织为50至250 CFU。通过透射电子显微镜未观察到李斯特菌细胞穿过派尔集合淋巴结和绒毛状肠的上皮层。扫描电子显微镜证实了李斯特菌与派尔集合淋巴结的滤泡相关上皮之间缺乏显著相互作用。派尔集合淋巴结的滤泡组织是李斯特菌复制的优先部位。在所有测试剂量下，派尔集合淋巴结中的细菌生长速率比绒毛状肠中的高10至20倍。在派尔集合淋巴结感染的早期阶段，在圆顶区域的单核细胞内观察到李斯特菌。然后，李斯特菌扩散至整个滤泡组织，但生发中心除外。完成此过程需要毒力决定因素hly以及程度较轻的actA，但不需要inlAB。这项研究表明，由于存在性质尚待确定的高度易感性单核细胞，派尔集合淋巴结是单核细胞增生李斯特菌复制而非进入的优先部位。
