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Gene expression profiles in gastric mucosa from a transgenic mice infected with H. pylori and immunized with BabA

ABSTRACT: Many vaccination studies have revealed various degrees of protection in mouse models. However, the mechanism of protection is not fully understood. The aim of this study was to identify genes specifically expressed in H. pylori infection and prophylactic immunized mice. A prophylactic immunization with purified protein of H. pylori BabA combining with the mucosal CTA1-DD adjuvant was performed in a-1,3/4-fucosyltransferase transgenic FVB/N mice. Gene expression profile was analysed from the gastric mucosa among untreated, the infected and immunized mice. There were a set of genes were upregulated or downregulated respectively, in infected mice as compared with untreated mice. These include the adipokines released form adipose tissue, adhesion molecules and actin cytoskeletal rearragemet associated genes. In immunized mice, however, the host response was not as strong as in infected mice and significantly changed genes were completely overlapped with those in infected mice. The expression data from genechip was confirmed by quantitative real-time PCR assay. The microarray analysis suggests that genes such as actin cytoskeletal molecules and adipokines may be as potential targets of H. pylori infection. Prophylactic immunization with purified protein of H. pylori BabA combining with the mucosal CTA1-DD adjuvant could reduce bacteria colonization without induced a severe degree of inflammation. Keywords: response to treatment

ORGANISM(S): Mus musculus

PROVIDER: GSE5398 | GEO | 2011/01/04

SECONDARY ACCESSION(S): PRJNA96295

REPOSITORIES: GEO

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Project description:Vaccination reduces morbidity and mortality from pneumonia but its effect on the tissue-level response to infection is still poorly understood. We evaluated pneumonia disease progression, acute phase response and lung gene expression profiles in mice inoculated intranasally with virulent gram-positive Streptococcus pneumoniae serotype (ST) 3, with and without prior immunization with pneumococcal polysaccharide ST 3 (PPS3), or co-immunization with PPS3 and with a low dose of lipopolysaccharide (LPS). Pneumonia severity was assessed in the acute phase, 5, 12, 24 and 48 h post-inoculation (p.i.) and the resolution phase of 7 days p.i. Primary PPS3 specific antibody production was upregulated and IgM binding to pneumococci increased in PPS3-immunized mice. Immunizations with PPS3 or PPS3 + LPS decreased bacterial recovery the lung and blood at 24 and 48 h and increased survival. Microarray analysis of whole lung RNA revealed significant changes in the acute phase protein serum amyloid A (SAA) between noninfected and infected mice, which were attenuated by immunization. SAA transcripts were higher in the liver and lungs of infected controls, and SAA protein was elevated in serum, but decreased in PPS3-immunized mice. Thus, during a virulent pneumonia infection, prior immunization with PPS3 in an IgM-dependent manner as well as co-immunization with PPS3 + LPS attenuated pneumonia severity and promoted resolution of infection, concomitant with significant regulation of cytokine gene expression in the lungs, and acute phase proteins in the lungs, liver and serum. Each lung RNA sample represented an individual mouse, creating biological repeats for each treatment. In-vivo treatments were as follows: non-infected lung (vehicle-immunized) control (n=5), infected lung (vehicle-immunized) control at 48 hr post-inoculation (n=5), PPS3 and LPS co-immunized lung at 48 hr post-inoculation (n=4) and PPS3 and LPS co-immunized lung at 7 days post-inoculation (n=4).

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Gene expression profiles in gastric mucosa from a transgenic mice infected with H. pylori and immunized with BabA

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