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, 139 (1), 43-7

Influence of Age and Duration of Infection on Bacterial Load and Immune Responses to Helicobacter Pylori Infection in a Murine Model

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Influence of Age and Duration of Infection on Bacterial Load and Immune Responses to Helicobacter Pylori Infection in a Murine Model

T Minoura et al. Clin Exp Immunol.

Abstract

Using a murine model, we previously showed that Helicobacter pylori infects and colonizes offspring via maternal transmission during the nursing period. The aim of this study was to investigate the influence of age and duration of infection on inflammatory and immune responses to H. pylori in infant and adult mice. During the breast-feeding period, the number of bacteria was significantly suppressed in 1-week-old mice infected with H. pylori at an early stage of nursing, compared with adult mice, suggesting that breast-milk induces such low colonization. In addition, these mice had weaker gastric inflammation, especially Th1 cytokine and humoral responses than in mice infected with H. pylori after weaning in spite of elevated levels of Th1 cytokines. Although infant mice showed low inflammatory responses against H. pylori, they produced H. pylori-specific antibodies following vaccination with oral or parenteral adjuvant. Our results suggest the importance of age at the time of primary infection on bacterial load, gastric inflammation and humoral responses in a murine model of H. pylori infection.

Figures

Fig. 1
Fig. 1
The load of colonized bacteria in group 1 (1-week-old) (○), group 2 (3-week-old) (◊) and group 3 (5-week-old) (□); bacterial culture and PCR negative mouse (•). Data are presented as geometric mean ± standard error of the mean. The bacterial load of group 1 was significantly lower than that of the other two groups at 1 week after infection (****P < 0·0001) and at 2 weeks after infection (**P < 0·01). *P < 0·05 and ***P < 0·001, compared with group 3.
Fig. 2
Fig. 2
(a) Gastritis scores. Scores were graded on a scale of 0–3. Values represent mean ± standard error (SEM) of each group of mice. group 1 (1-week-old) (•), group 2 (3-week-old) (♦) and group 3 (5-week-old) (▪)*P < 0·05, **P < 0·01, ****P < 0·0001, compared with group 3, by analysis of variance with Tukey-Kramer's HSD test. (b) Comparison of production of gastric proinflammatory cytokines between group 1 (•) and group 4 (control mice) (○). *P < 0·05, **P < 0·01 and ****P < 0·0001, compared with the corresponding cytokine level of group 4, by the unpaired t-test.
Fig. 3
Fig. 3
IgG and IgA anti-H. pylori antibody titres in infected and immunized mice. (a) Closed symbols (•, ♦, ▪) are the geometric mean ± standard error (SEM) of each infection group. Analysis of variance with Tukey-Kramer's HSD test was used to compare differences in antibody titre. After 4 weeks post infection, IgG and IgA titres of group 1 were significantly lower than those of the other two groups (**P < 0·01; ***P < 0·001; *P < 0·05). IgG titres of group 2 were lower than those of the other two groups (*P < 0·05) at 8 weeks after infection. (b) Antibody production in 1-week-old mice after infection (▪), mucosal vaccination (formula image) and parenteral vaccination (formula image). Data are mean ± SEM. *P < 0·05; **P < 0·01; ****P < 0·0001, by the unpaired t-test.

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