A Listeria adhesion protein-deficient Listeria monocytogenes strain shows reduced adhesion primarily to intestinal cell lines
A Listeria adhesion protein-deficient Listeria monocytogenes strain shows reduced adhesion primarily to intestinal cell lines
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DOI：
10.1007/s00430-002-0150-1
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发表时间：
2003-05-01
影响因子：
5.4
通讯作者：
Bhunia, AK
中科院分区：
文献类型：
--
作者：
Jaradat, ZW;Wampler, JL;Bhunia, AK
单核细胞增生李斯特菌粘附并穿透肠细胞内膜引起全身感染。来自单核增生李斯特菌的一种104 kda的李斯特菌粘附蛋白（LAP）先前被证明与肠道肠细胞样Caco-2细胞的粘附有关。我们研究了一株lap缺陷突变株单核增生乳杆菌（A572）对多种人类肠道和非肠道细胞系的粘附和侵袭特性，以评估可能的靶宿主细胞。在肠道细胞系中，A572对回肠-盲肠（HCT-8）和结肠（Caco-2和HT-29）细胞的粘附性明显低于野生型（WT），而A572与野生型（WT）对其他来自十二指肠（HuTu-80）和空肠（Int-407）的肠道细胞系的粘附性无显著差异。在肝、肾、膀胱、卵巢、子宫颈、乳腺等非肠细胞系中，A572与WT的粘附性差异不大或无差异。喉部或皮肤。侵袭数据表明，A572具有侵袭性，但其侵袭效率与其对各细胞系的粘附特性成正比。在小鼠生物测定中，口服给药后肝脏中未发现A572，提示LAP突变体可能无法通过肠细胞壁。免疫电镜显示，LAP定位于细菌表面和细胞质。在总结。本研究提示，lap介导的黏附与来自小肠下部和大肠上部的肠细胞有关，并可能在感染的肠期发挥重要作用。
Listeria monocytogenes adheres and penetrates intestinal cell linings for systemic infection. A 104-kDa Listeria adhesion protein (LAP) from L. monocytogenes was previously demonstrated to be responsible for adhesion to intestinal enterocyte-like Caco-2 cells. We investigated the adhesion and invasion characteristics of a LAP-deficient mutant L. monocytogenes strain (A572) to various human intestinal and non-intestinal cell lines to assess the possible target host cells. Among the intestinal cell lines, A572 showed significantly reduced adhesion than the wild type (WT) strain to the cells of ileum-cecum (HCT-8) and colon (Caco-2 and HT-29), whereas A572 and WT did not show any significant differences in adhesion to other intestinal cell lines from duodenum (HuTu-80) or jejunum (Int-407). Differences in adhesion between A572 and WT were little or none in non-intestinal cell lines from liver, kidney, bladder, ovary, cervix, breast.. larynx, or skin. Invasion data showed that A572 was invasive but the invasion efficiency was proportional to its adhesion characteristics to respective cell lines. In mouse bioassay, A572 was not found in liver following oral administration, suggesting that LAP mutant was possibly unable to pass through intestinal cell linings. Immuno-electron microscopy revealed that the LAP is localized in the bacterial surface as well as the cytoplasm. In summary., this study indicated that the LAP-mediated adhesion is associated with the intestinal cells originating from the lower part of small intestine and from the upper part of large intestine, and possibly plays an important role during the intestinal phase of infection.