pylori challenge. A similar approach used a Salmonella vector construct that expressed fusion proteins complexed with H. pylori CagA, VacA, and UreB in different arrangements.

Oral therapeutic immunization of mice with this candidate vaccine significantly decreased H. pylori colonization in the stomach; protection was related to the combination of Th1, serum IgG, and mucosal IgA responses [41]. Guo et al. [42] used an E. coli expressed fusion protein construct of cholera toxin B subunit and a UreA epitope of H. pylori urease A vaccine had good immunogenicity and immunoreactivity and could induce specific neutralizing antibodies; however, the efficiency of the vaccine should be confirmed by a sterilizing immunity trial because urease-targeting vaccines have a long history of disappointing Selumetinib mw results. Nevertheless, it is worth to mention an epitope urease vaccine developed by Chen et al. [43]. The UreB was effectively expressed as food-grade antigen in Lactococcus lactis where the achieved percentage of recombinant antigen was estimated to be 7% of total soluble cellular proteins. Similar UreB gene expression, but in peanut, was achieved by Yang et al. [44] where UreB gene was transformed into peanut embryo leaflets by an Agrobacterium-mediated method. Both approaches could serve as

alternative vaccine strategies for preventing H. pylori infection. It is also worth mentioning some vaccination experiments not directed toward novel approaches in vaccine production, KU-57788 chemical structure but being important click here to further elucidate vaccination response against H. pylori. In a fascinating work from DeLyria et al. [45], IL-17A and IL-17A receptor knockout mice were immunized with H. pylori sonicate and cholera toxin as adjuvant. Surprisingly, despite the previous demonstration that IL-17 antibody-mediated neutralization during challenge of mice compromises the protective immune response [46], the complete absence of IL-17A or its receptor

did not significantly impact the ability of the murine host to develop vaccine-induced protective immunity against H. pylori or H. felis. Although the IL-17 response may be important for the eradication of the bacteria, as previously observed, there are multiple mechanisms for activating vaccine-based protective inflammatory responses against H. pylori that employ compensatory mechanisms of immunity. In conclusion, progress in vaccine development has been made in the past year. Several new approaches were taken, including novel T-cell epitopes and virulence factors delivered with an IL-2 gene-encoded construct. H. pylori virulence factor vaccines appear to be effective in mouse models, including urease, NAP, and OipA. Surprisingly, IL-17 was not shown to play an important role in protective immunity against H. pylori.