Research Projects

N. meningitidis is a unique pathogen that is adapted to the human host, with no repertoire in other animals. The factors affecting host adaptation and the transition from asymptomatic to symptomatic infection are still unknown. The extracellular pool of polyamines within the host environment could potentially affect N. meningitidis' virulence, as it lacks polyamine synthesis machinery and relies on transport from the extracellular pool. A previous study showed that spermidine and spermine upregulate capsule synthesis in N. meningitidis, which enhances its survival in macrophages. However, the molecular mechanisms involved are not yet understood. The current knowledge includes that N. meningitidis adherence and microcolony dispersal play a significant role in its pathogenesis, but the signaling factors contributing to these factors are not fully understood. Additionally, capsular switching results in vaccine and therapeutic failure, but the factors contributing to this switch are not yet deciphered. N. meningitidis is restricted to the human host, confined to respiratory tract infections, but has now been involved in urogenital tract infections. Understanding the molecular mechanisms resulting in the evolution of N. meningitidis to invade tissues other than the respiratory tract is crucial for future research. The findings will provide evidence that the extracellular pool of polyamines regulates N. meningitidis' virulence, which can be further validated using mice models. Understanding the mechanism of polaymine signaling interference with virulence will help identify novel targets to combat Neisseria spp. pathogenesis, identify polyamine modulon of virulence in N. meningitidis, and fill gaps in understanding symptomatic and asymptomatic infections in N. meningitidis pathogenesis.