Giampaglia C M, da Silva M L
Instituto Adolfo Lutz, Coleção de Culturas, São Paulo.
Arq Gastroenterol. 1991 Apr-Jun;28(2):69-75.
Adherence of enteropathogenic Escherichia coli (EPEC) to enterocytes with subsequent destruction of microvilli is supposed to be their mechanism of virulence. Adhesion may be studied in vitro systems using HeLa or HEp-2 cells, to which EPEC adhere in a localized pattern. We show here that colostrum and human milk inhibit E. coli 0111ab:H2 adherence to HeLa cells in different experimental conditions. Lactose does not seem to be involved in the in vitro inhibition since no effect was observed when a concentration of 7.5% was used during the test. A bacterial growth curve performed in same conditions of adherence test showed no bacteriostatic effect of human milk. S-IgA and receptor analogues could be responsible for the adherence inhibition observed.
肠致病性大肠杆菌（EPEC）黏附于肠上皮细胞并随后破坏微绒毛被认为是其致病机制。黏附作用可以在体外系统中使用HeLa或HEp - 2细胞进行研究，EPEC以局部模式黏附于这些细胞。我们在此表明，在不同实验条件下，初乳和人乳可抑制大肠杆菌O111ab:H2对HeLa细胞的黏附。乳糖似乎不参与体外抑制作用，因为在试验中使用7.5%的浓度时未观察到效果。在与黏附试验相同条件下进行的细菌生长曲线显示人乳没有抑菌作用。观察到的黏附抑制作用可能由分泌型免疫球蛋白A（S - IgA）和受体类似物引起。
