Preparation, characterizations and in vitro cytotoxic activity of nickel oxide nanoparticles on HT-29 and SW620 colon cancer cell lines.

Despite the extensive implication of nickel oxide nanoparticles (NiO-NPs) in different fields such as biomedical science and industrial manufacturing, their effect on human cancer cells has not been elucidated. In this study, we report a simple process for the preparation of NiO-NPs. X-ray diffraction and transmission electron microscopy were used to characterize the surface architecture and dimension of the synthesized NiO-NPs. The average diameter of the NiO-NPs was approximately 20-25 nm. We used two human colon cancer cell lines, HT-29 and SW620, to assess the nanoparticles' cytotoxicity. The MTT assay showed that the NiO-NPs reduced cell viability of HT-29 and SW620 cell lines. The results of inverted microscopy showed the highest cytotoxic activity with 600 µg/ml concentration of NiO-NPs on HT-29 cells. Western blot assay showed the downregulation of anti-apoptotic Bcl2 and Bcl-xL proteins in HT-29 cells treated with NiO-NPs. Moreover the results demonstrated the induction of PARP (Cleaved) in NiO-NPs treated HT-29 cells which are considered the marker of apoptosis. The NiO-NPs were not demonstrated bactericidal effect on six different bacterial strains tested, implying that the NiO-NPs may not perturb the human normal gut microbiome. The results have showed the promising application of the NiO-NPs in management of cancer in near future.

Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease.

Hosts and microbes have co-evolved over millions of years. Inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic immune-mediated diseases. Although the etiology of IBD remains an enigma, various studies have proposed the involvement of mucosa-associated Escherichia coli (E. coli) strains in the pathogenesis of IBD. E. coli, a usual inhabitant of the intestine, causes disease after acquiring virulence factors; however, the mechanisms underlying this phenomenon are not well understood. In the present review, we will discuss recent findings on how gut E. coli regulates and controls gut homeostasis and the pathogenesis of IBD. We will also summarize current knowledge regarding the cause, mechanism, genetics, and environmental factors involved in the regulation of IBD. Furthermore, we will discuss the possibility of alterations in innate and acquired immunity during the course of disease as well as possible treatment.