The inhibition of gene expression, although occurring in some cases, has been little studied. In relation to the insect��s resistance to insecticides, the response of some P450 inhibitors has been studied from the point of view of the synergists of the insecticides. The results of the present study support the hypothesis that feeding on a Bt diet causes an suppression in the P450 expression, then reduces the feeding activity, and then the expression increases slightly and so does the feeding activity, so growth is more limited and slower. Mao et al demonstrated that the larvae of H. armigera fed on transgenic cotton plants expressing dsCYP6AE14 showed a SCH772984 ERK inhibitor reduced expression level of CYP6AE14 and drastically retarded growth, so the effect achieved with the gene suppression by the dsRNA plants was somewhat similar to the effect produced by the gene suppression by the Bt toxin. It must be pointed out that the response of the P450 genes of insects to Bt ingestion has been studied very little. H. armigera larvae have developed resistance to many Wortmannin side effects insecticides and to the Cry1Ac toxin in a Bt cotton in field in China, and have been reported to be tolerant to Bt maize in Europe. The unexpected suppressive effect of the Cry1Ab toxin in the P450 genes of the CYP6 and CYP9 families of H. armigera larvae deserves to be further studied in order to determine whether the response to other Cry toxins is similar, whether the suppressive effect of the toxin can act as a synergist for other xenobiotics or other Cry toxins, how the strains of H. armigera resistant to insecticides respond to Bt toxins, and whether this response is related in some way to the low tolerance of the species to the Bt toxin. Crohn��s disease and ulcerative colitis are the two major forms of idiopathic inflammatory bowel disease, with a combined prevalence of about 150�C200 cases per 100,000 in Western countries. They are multifactorial diseases, occurring in individuals with genetic predisposition in whom an environmental or infectious trigger causes an abnormal immune response. Several lines of evidence suggest that bacteria play a role in the onset and perpetuation of IBD. Intestinal bacteria are essential for the development of intestinal inflammation.