In this study, we found a positive correlation between IL-1b production and cytotoxicity induced by EHEC-Ehx. Even the cytotoxicity of Ehx has been found to contribute to the release of IL-1b through cell lysis, which cannot be the main source of extracellular IL-1b because most of the IL-1b in the supernatant was biologically active mature IL-1b, as shown by immunoblot analysis. Further experiments are needed to determine the mechanism by which cytotoxicity of Ehx affects the secretion of mature IL-1b into the extracellular space and how cytotoxic Ehx affects the pathogenesis of EHEC infection. In this study, we found EHEC O157:H7-Ehx to contribute to cytotoxicity in THP-1 cells. It was also found responsible for higher levels of mature IL-1b. The NLRP3 inflammasome was found to mediate EHEC O157:H7-activated IL-1b production. Ehx may activate pro-caspase-1 through activation of NLRP3, like other pore-form bacteria toxins. However, the possibility that other types of inflammasome signaling may be activated by Ehx cannot yet be ruled out. This may also have stimulated the release of IL-1b. Cytotoxicity to THP-1 cells may also contribute to the release of IL-1b using some as yet unknown mechanism. Further study is needed to determine the possible roles of IL-1b in the pathogenesis of this potentially fatal foodborne infection. Genomic imprinting is an epigenetic phenomenon observed in eutherian mammals. For the large majority of autosomal genes, the two parental copies are both either transcribed or silent. However, in a small group of genes one copy is turned off in a parent-of-origin specific manner thereby resulting in monoallelic expression. These genes are called ‘imprinted’ because the silenced copy of the gene is epigenetically marked or imprinted in either the egg or the sperm. Imprinted genes play important roles in development and growth both pre- and Staurosporine postnatally by acting in fetal and placental tissues. Interestingly, there appears to exist a general pattern whereby maternally expressed genes tend to limit embryonic growth and paternally expressed genes tend to promote growth. A model case for this striking scenario is the antagonistic action of Igf2 and Igf2r in mouse. Deletion of the paternally expressed Igf2 gene results in intrauterine growth restriction. On the other hand, deletion of the maternally expressed gene Igf2r, results in overgrowth. The observation that maternally and paternally expressed genes apparently act as antagonists has inspired several evolutionary theories that aim to explain the origin of genetic imprinting under the process of ‘natural selection’. The most scientifically accepted theory is currently the kinship theory and. Briefly, this theory suggests that in polygamous mammalian species, silencing of maternally derived growth inhibiting genes results in increased growth of the embryo. This is associated with an increased nutritional demand and thereby with an exploitation of maternal resources at the cost of future off-spring that might be fathered by a different male. The evolution of a gene regulatory mechanism that silences preferentially one parental allele of a gene implies that paternally and maternally expressed genes experience different selective pressures during evolution. This assumption is supported by the finding that the two groups reveal different patterns of sequence conservation. Whereas the protein-encoding DNA sequences of paternally expressed genes are well conserved among different mammalian species, maternally expressed genes are much more divergent. Whether paternally and maternally expressed genes differ also in molecular functions and gene regulation is a question that has not yet been investigated in detail.