Streptococcus pneumoniae is a gram positive, facultative anaerobic bacterium and is the leading bacterial cause of pneumonia, meningitis and sepsis [1]. Upon infection by the bacterial pathogen S. pneumoniae, the host innate immune response oversaturates the infection site with high concentrations of zinc causing a phenomenon called zinc toxicity.
The molecular basis of Zn toxicity in S. pneumoniae, is still currently being elucidated. One well-established mechanism involves the inhibition of Mn2+ uptake by Zn2+ through its irreversibly binding to the PsaBCA transporter [2]. Zn toxicity is known to increase oxidative stress in S. pneumoniae due to the inhibition of Mn uptake [3]. However, it is also known that Zn toxicity can causee oxidative stress via disruptions of many intracellular pathways [3], implying that the metal has additional mechanisms of action beyond its inhibition of Mn2+ transport.
This poster will present our recent progress in the characterization of intracellular targets of metal toxicity and the specific mechanisms of action, both from a structural and functional point of view.