ASF) or C57BL/6 specific pathogen free mice (B6.SPF) with H. felis. After 24 weeks, both groups progressed to gastric dysplasia, but B6.SPF mice displayed decreased H. felis colonisation and acquisition of multiple new bacterial species. Potential mechanisms responsible for the ineffective H. felis clearance in the B6.ASF model Selleckchem Cabozantinib include the absence of new gastric microbiota, the lack of expression of new gastric mucins, and a reduced ratio of H. felis–specific IgG2c:IgG1 serum antibodies. Zhang et al. [42] reported that the administration

of Lactobacillus salivarius REN to F344 rats counteracts the unfavorable 4-nitroquinoline-1-oxide-induced changes in colonic microbiota by its suppressive effect on Helicobacter spp. On the contrary, Whary et al. [43] observed that the development of typhlocolitis in H. hepaticus-infected B6.129P2-IL-10tm/Cgn (IL-10−/−) mice required co-colonisation with L. reuteri. These data contrast with previous reports by the same group showing that intestinal lesions are attenuated in H. hepaticus/L. reuteri 6798 or H. hepaticus/L. paracasei coinfected SPF B6.129 IL-10−/−

mice. However, Büchler et al. [44] Deforolimus supplier revealed that strain-specific enterocolitis susceptibility in IL-10−/− mice depends on a complex interplay between host genetics and gut microbiota composition. The authors claimed that single pathogens (i.e., H. hepaticus) are not sufficient to determine whether IBD susceptibility or resistance is fully displayed. A new species-specific qPCR assay based on cdtB (cytolethal distending toxin B) was developed to detect H. pullorum in tissue and feces of infected mice [36]. A molecular enrichment strategy based on class specific amplification of the cpn10-cpn60 operon was developed for the detection of Epsilon-proteobacteria in the dog fecal microbiome, allowing the amplification of two possible novel Helicobacter spp. [45]. A combined agar and broth dilution method was developed to determinate

the antimicrobial susceptibility of H. suis [46]. check details Finally, a review describing laboratory procedures for culture and maintenance of Helicobacter spp. was published last year [47]. Over the last year, significant advances have been made in the understanding of the biology of NHPH species, their interaction with the host, the molecular basis of transmission to humans and their potential pathogenicity for both humans and animals. Conflict of Interest: the authors have declared no conflict of interest;][#,63]?> “
“Outer inflammatory protein A (OipA) has an important role in Helicobacter pylori pathogenesis. In this study, we purified the outer membrane protein and evaluated the effects of this protein on maturation and cytokine production by dendritic cells (DCs). The oipA gene was inserted into pET28a, and this construct was transformed into Escherichia coli BL21 (DE3). Purification of the recombinant protein was performed by Ni-NTA affinity chromatography.