When the survival curves of the three groups of infected mice wer

When the survival curves of the three groups of infected mice were compared, the Kaplan Meier statistic was not significant (P = 0.105). In experiment 5 (diet comparison), levels of gross pathology in infected mice were similar learn more in all groups of mice (Figure 8C); no control mice exhibited gross pathology. When gross pathology scores of the six groups of mice were analyzed using two-way ANOVA on ranked data, differences among the groups due to infection status were significant (Pcontrols vs infected = 6.11 × 10-24), but there was no statistically significant difference due to diet (P = 0.956), nor was there a statistically significant

interaction between infection status and diet (P = 0.956). Histopathology scores were elevated both in infected mice kept on the ~6% fat diet throughout and in infected mice experiencing the transition from the ~12% fat diet to the ~6% fat diet (Figure

8D). When histopathology scores of the six groups of mice were analyzed using two-way ANOVA on ranked data, differences among the groups due to infection status were significant (Pcontrols vs infected = 2.33 × 10-6), but there was no statistically significant difference due to diet (P = 0.553). Nor was there a statistically significant interaction between infection status and diet (P = 0.611). Humoral immune responses to C. jejuni IWR-1 cell line infection of mice on the different dietary regimes in experiment 5 (diet comparison) are shown in Figure 9. When two-way ANOVA was conducted on these data, the effect of infection status (infected vs controls) was significant for plasma levels of anti-C. jejuni IgG2b, IgG2c, IgG3, and IgA (P = 1.68 × 10-10, 8.93 × 10-7, 8.57 × 10-7, and 5.34 × 10-6, respectively) but not for IgG1 (P = 0.109). There was no statistically significant effect of diet on levels of anti-C. jejuni IgG2b, IgG2c, IgG3, or IgG1 (P = 0.114, 0.203, 0.204, and 0.477, respectively). There was no statistically significant

interaction between diet and infection status for anti-C. jejuni IgG2b, IgG2c, IgG3, or IgG1 (P = 0.202, 0.075, 0.076, and 0.620, respectively). However, for plasma anti-C. jejuni IgA, there was a statistically Resveratrol significant effect of diet (P = 0.012) as well as a significant interaction between diet and infection status (P = 0.035). Plasma IgA levels were significantly different in mice on the ~6% fat diet compared to mice on the ~12% fat diet (Pcorrected = 0.019) and in mice on the ~6% fat diet compared to mice experiencing the transition between the two diets at the time of inoculation (Pcorrected = 0.032). Plasma IgA levels in mice experiencing the dietary transition were not significantly different from those of mice on ~12% fat diet (P = 0.695). Figure 9 Plasma anti- C. jejuni antibody levels in mice on different dietary regimes (experiment 5).

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