Figure 6. Helix 30 of LtgA plays a role in N.meningitidis host adaptation and virulence.

N.meningitidis wild-type, ΔltgA, ΔltgA^ltgA and ΔltgA^ltgAΔ30 were administered to transgenic mice expressing human transferrin via an intraperitoneal route. (a) Bacterial burden was determined by enumeration of CFUs in blood 2, 6 and 24 hr pi. These data show that the strain complemented with a deletion in helix 30 is cleared faster than the other strains. (b) Pro-inflammatory cytokine (IL-6) and chemokine (KC) profile in blood of infected mice was evaluated 2, 6 and 24 hr post-infection by ELISA. The ΔltgA^ltgAΔ30 strain induced the production of lower levels of inflammatory mediators production upon infection compared to the other strains. Data represent three independent experiments with n = 5. Statistical analysis was done by Kruskal-Wallis non-parametric comparison against the complemented strain with a p-value<0.01.