Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Biol Res. 2012;45(1):21-6. doi: 10.4067/S0716-97602012000100003.
Shigella flexneri causes bacillary dysentery in humans. Essential to the establishment of the disease is the invasion of the colonic epithelial cells. Here we investigated the role of the lipopolysaccharide (LPS) O antigen in the ability of S. flexneri to adhere to and invade polarized Caco-2 cells. The S. flexneri 2a O antigen has two preferred chain lengths: a short O antigen (S-OAg) regulated by the WzzB protein and a very long O antigen (VL-OAg) regulated by Wzz pHS2. Mutants with defined deletions of the genes required for O-antigen assembly and polymerization were constructed and assayed for their abilities to adhere to and enter cultured epithelial cells. The results show that both VL- and S-OAg are required for invasion through the basolateral cell membrane. In contrast, the absence of O antigen does not impair adhesion. Purified LPS does not act as a competitor for the invasion of Caco-2 cells by the wild-type strain, suggesting that LPS is not directly involved in the internalization process by epithelial cells.
福氏志贺菌会导致人类细菌性痢疾。该疾病的建立的关键是结肠上皮细胞的入侵。在此，我们研究了脂多糖（LPS）O 抗原在福氏志贺菌黏附和侵袭极化的 Caco-2 细胞的能力中的作用。福氏志贺菌 2a 型 O 抗原有两种偏好的链长：由 WzzB 蛋白调控的短 O 抗原（S-OAg）和由 Wzz pHS2 调控的非常长的 O 抗原（VL-OAg）。构建了缺失 O 抗原组装和聚合所需基因的明确缺失突变体，并检测了它们黏附和进入培养上皮细胞的能力。结果表明，VL-OAg 和 S-OAg 都需要穿过基底外侧细胞膜进行入侵。相比之下，缺失 O 抗原不会损害黏附。纯化的 LPS 不能作为野生型菌株入侵 Caco-2 细胞的竞争物，表明 LPS 不直接参与上皮细胞的内化过程。
