Karunasagar I, Senghaas B, Krohne G, Goebel W
Lehrstuhl Mikrobiologie, Theodor-Boveri-Institut für Biowissenschaften, Würzburg, Germany.
Infect Immun. 1994 Aug;62(8):3554-8. doi: 10.1128/iai.62.8.3554-3558.1994.
Evidence that Listeria monocytogenes enters Caco-2 cells through the apical surface is presented. Attachment of bacteria to host cells seems to induce modifications of microvilli which are either in direct contact with the bacterial surface or in close vicinity, resulting in the formation of lamellipodia involved in the cellular uptake of the bacteria. Such modifications are not induced by L. monocytogenes SLCC 53, which carries a deletion in the prfA gene, although attachment of this mutant to Caco-2 cells occurs. Listeria innocua does not attach well to Caco-2 cells and also fails to cause structural alterations of the microvilli. Treatment of confluent monolayers of Caco-2 cells with ethylene glycol-bis(beta-aminoethyl ether)- N,N,N1,N1-tetraacetic acid (EGTA), which disrupts intercellular junctions, greatly reduced the uptake of Listeria cells. Attachment and invasion of L. monocytogenes was not accompanied by accumulation of filamentous actin around the entering bacterial cell.
本文提供了单核细胞增生李斯特菌通过顶端表面进入Caco-2细胞的证据。细菌与宿主细胞的附着似乎会诱导与细菌表面直接接触或紧邻的微绒毛发生改变,导致形成参与细菌细胞摄取的片状伪足。单核细胞增生李斯特菌SLCC 53(其prfA基因存在缺失)虽能与Caco-2细胞附着,但不会诱导此类改变。无害李斯特菌与Caco-2细胞的附着性不佳,也不会引起微绒毛的结构改变。用乙二醇双(β-氨基乙基醚)-N,N,N',N'-四乙酸(EGTA)处理汇合的Caco-2细胞单层(EGTA会破坏细胞间连接),会大大降低李斯特菌细胞的摄取。单核细胞增生李斯特菌的附着和侵入并未伴随丝状肌动蛋白在进入细菌细胞周围的积累。