Another study around the adaption of to acidic stress reported that HP1286 expression is usually strongly up regulated in a UreI-negative strain, a mutant unable to transport urea inside the cell (Toledo et al., 2002). an inhibitor of the ERK MAPK signaling pathway significantly reduced rHP1286-induced apoptosis. Furthermore, nuclear translocation of ERK and phosphorylation of c-Fos was detected in rHP1286-treated macrophages. These results provide functional insight into the potential role of HP1286 during contamination. Considering the ability of HP1286 to induce macrophage apoptosis, the protein could possibly help in the bacterial escape from your activated macrophages and persistence in the belly. is known to selectively colonize the human gastric mucosa for over 50,000 years. Currently, more than half of the world’s populace is usually colonized by through several strategies, such as phagocytosis, production of various cytokines/chemokines, and microbicidal compounds such as ROS and NO (Wilson et al., 1996; Gobert et al., 2002a,b). However, is known to block or regulate these macrophage strategies, which results in inefficient bacterial killing. Induction of programmed cell death or apoptosis in macrophages is Bendroflumethiazide usually a well-known bacterial strategy that helps in the colonization and persistence of the bacterium. It has been reported Bendroflumethiazide previously that or bacterium-derived products induce apoptosis in macrophages, which occurs Bendroflumethiazide via polyamine-dependent mechanisms and signaling via ERK-MAPK and the Src family of tyrosine kinases (Allen et al., 2000; Zheng and Jones, 2003; Chaturvedi et al., 2004; Asim et al., 2010; Pathak et al., 2013). Despite the small size of the genome, a large portion, presumably from 30 to 40%, is usually annotated as hypothetical proteins with unknown Bendroflumethiazide function (Zanotti and Cendron, LRCH1 2014). Among this group, many are secreted by the bacterium. Based on numerous studies, the secretome appears to be composed of approximately 160 proteins (Zanotti and Cendron, 2014). Considering the general noninvasive nature of whose role Bendroflumethiazide in bacterial pathogenesis remains unidentified. With this in view, this study was focused on functional characterization of the protein HP1286. Presence of HP1286 in the external medium of culture has been reported in several independent studies (Bumann, 2002; Kim et al., 2002; Mller et al., 2013). Crystal structure analysis led to the placement of HP1286 in the family of YceI-like proteins, due to the presence of a cavity created by an eight-stranded -barrel (Sisinni et al., 2010). However, based on the structure and shape of the internal cavity, which varies from other members of the family, it was suggested that HP1286 has the function of binding and/or transporting amphiphilic molecules (Sisinni et al., 2010). Another study around the adaption of to acidic stress reported that HP1286 expression is usually strongly up regulated in a UreI-negative strain, a mutant unable to transport urea inside the cell (Toledo et al., 2002). In addition, a recent study showed that recombinant HP1286 induces apoptosis in gastric epithelial cell collection AGS (Li et al., 2012). The balance between cell death and cell growth is essential for the normal function of gastric mucosa. By induction of apoptosis in gastric epithelial cells, HP1286 along with other known apoptosis-inducing factors of (Kuck et al., 2001; Basak et al., 2005; Kim et al., 2007) could eventually damage the gastric epithelial cell layer, allowing the conversation of HP1286 and other virulence factors with numerous immune cells in the lamina propria. In this study, we have analyzed the apoptosis-inducing ability of HP1286 on other possible target cells such as macrophages, monocytes, neutrophils, and T cells. We provide evidence indicating that although rHP1286 interacts with several immune cells, it is capable of inducing apoptosis.