Group B
Streptococcus (GBS) causes
meningitis in
neonates and
Nile tilapia (
Oreochromis niloticus). The molecular mechanisms regulating the intracellular
survival of this pathogen in the host
cell are complex and crucial for the progression of
infection. Thus, we propose the use of GBS-infected
Nile tilapia microglia as an
in vitro model system simulating
infection caused by homologous
bacteria in
humans. We used this model to evaluate the phagocytic activity, as well as the functional aspects of the capsular
proteins A, B, C, and D and the major
redox enzymes, and the synergistic
role of mechanisms/
proteins involved in blocking phagocytic process. We observed that in the intracellular phase, GBS showed enhanced synthesis of the
polysaccharide capsule and used
superoxide dismutase,
thioredoxin,
NADH oxidase, and
alkyl hydroperoxide reductase to scavenge
reactive oxygen species and
reactive nitrogen species produced by the host
cell. Furthermore, although these
virulence mechanisms were effective during the initial hours of
infection, they were not able to subvert microglial responses, which partially neutralized the
infection. Altogether, our findings provided important information regarding the intracellular
survival mechanisms of GBS and perspectives for the
production of
new drugs and
vaccines, through the druggability
analysis of specific
proteins. In conclusion,
tilapia microglia serve as a potent
in vitro experimental model for the study of
meningitis.