Shiga toxins (Stxs), some of the most important virulence factors in enterohemorrhagic Escherichia coli (EHEC) O157:H7, are known to be induced and released by various environmental cues, such as DNA damage responses and stress-inducing chemicals. In order to investigate the possible effects of growth media on Stxs expression, we analyzed the growth kinetics and expression of Stxs (Stx1 and 2) in cells grown in Luria-Bertani (LB) and E. coli (EC) media, which are widely used for EHEC O157:H7. Through direct plating and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), it was revealed that, when EHEC O157:H7 was grown in EC medium, the total bacterial count was reduced significantly and the stx1 transcription was greatly increased during the stationary growth phase than that in LB. Here we report that bile salts and lactose, which are the two only components in EC medium that are absent in LB, function as negative and positive regulatory signals, respectively, for the transcription of both stx1 and stx2. Indeed, stx transcription was significantly increased (~5.7 and ~21.8 fold for stx1 and stx2, respectively; p < 0.05) in an EC medium lacking bile salts when compared to the normal EC. In contrast, EHEC O157:H7 grown in an EC medium lacking lactose did significantly decrease these transcriptions (~93.5 and ~4.3 fold for stx1 and stx2, respectively; p < 0.05). Consistently, stx transcription was drastically increased in an LB medium supplemented with lactose, implying that lactose might be an environmental trigger for the expression of Stxs.

Lactose is a disaccharide consisting of a glucose and a galactose. Milk is a sole source of lactose in natural food. Lactase hydrolyzes lactose into glucose and galactose, which are absorbed in the intestine and utilized by the body. After weaning, lactase activity declines. Therefore, the majority of adults have hypolactasia. The prevalence is above 50% in South America, Africa, and Asia. A significant amount of lactose is consumed as cow milk-based food products. However, it has no special nutritional importance for adults, and it is suspected as a dietary risk factor for coronary heart disease (CHD) and ovarian cancer. The aim of this study is to review the evidence and to propose possible mechanisms regarding the relations between lactose intake and CHD and ovarian cancer. Epidemiological studies support the connection of lactose and CHD. Although several mechanisms for elucidation of this connection have been suggested, calcium theory is the most plausible. Galactose is known to be toxic to ovary. Galactose has been suggested to induce ovarian cancer through hypergonadotropic hypogonadism. Some epidemiological data support this but others do not. Consumption of lactose or galactose can induce CHD and ovarian cancer; however, more research will be needed in order to determine the relation between lactose and these diseases.