Centro de Investigación y Desarrollo en Criotecnología de Alimentos (Consejo Nacional de Investigaciones Científicas y Técnicas [CONICET], La Plata), Calle 47 y 116-B1900AJI, La Plata, Argentina.
J Food Prot. 2013 May;76(5):820-6. doi: 10.4315/0362-028X.JFP-12-294.
Bacillus cereus interaction with cultured human enterocytes and the signaling pathways responsible for the biological effects of the infection were investigated. Results demonstrate that calcium depletion increases the ability of strains T1 and 2 to invade cells. Bacteria associated in greater extent to undifferentiated enterocytes and extracellular factors from strain 2 increased its own association and invasion. Inhibitors of signaling pathways related to phosphorylated lipids (U73122 and wortmannin) were able to significantly reduce cytoskeleton disruption induced by B. cereus infection. Adhesion of strain T1 decreased in the presence of U73122 and of wortmannin, as well as when those inhibitors were used together. In contrast, invasion values were diminished only by U73122. Results show that different factors are involved in the interaction between B. cereus and cultured human enterocytes. Following infection, disruption of the cytoskeleton could facilitate invasion of the eukaryotic cells.
研究了蜡样芽胞杆菌与培养的人肠细胞的相互作用以及感染的生物学效应所涉及的信号通路。结果表明，钙耗竭增加了菌株 T1 和 2 侵袭细胞的能力。与未分化肠细胞结合更紧密的细菌，以及来自菌株 2 的细胞外因子，增加了其自身的结合和侵袭能力。与磷酸化脂质相关的信号通路抑制剂（U73122 和wortmannin）能够显著减少蜡样芽胞杆菌感染引起的细胞骨架破坏。在 U73122 和wortmannin 的存在下，以及当同时使用这两种抑制剂时，菌株 T1 的粘附减少。相比之下，只有 U73122 降低了侵袭值。结果表明，不同的因素参与了蜡样芽胞杆菌与培养的人肠细胞之间的相互作用。感染后，细胞骨架的破坏可能促进真核细胞的入侵。
