The success of Staphylococcus aureus as a pathogen is partly attributable to its ability to thwart host innate immune responses, which includes resisting the antimicrobial functions of phagocytes. Macrophages are key phagocytic cells that typically eradicate infecting pathogens - however, research from the Heinrichs Lab demonstrates that macrophages fail to control intracellular infection by MRSA. Indeed, intracellular staphylococci proliferate while the bacteria are residing in mature phagolysosomes hours after initial phagocytosis.
The Heinrichs Lab investigates the interaction between S. aureus and macrophages to understand the host-microbe interactions influence the outcome of infection. Using a wide array of fluorescent-based imaging tools, the lab aims to answer the following questions:
how do macrophages restrict mrsa's access to nutrients?
how does mrsa obtain nutrients during intracellular growth?
how does mrsa resist the antimicrobial functions of macrophages?
Flannagan RS, Kuiack RC, McGavin MJ, Heinrichs DE. 2018. Staphylococcus aureus uses the GraXRS regulatory system to sense and adapt to the acidified phagolysosome in macrophages. mBio. Jul 17;9(4). pii: e01143-18. doi: 10.1128/mBio.01143-18.
Flannagan RS, Watson DW, Surewaard BG, Kubes P, Heinrichs DE. 2018. The surreptitious survival of the emerging pathogen Staphylococcus lugdunensis within macrophages as an immune evasion strategy. Cell Microbiol. 2018 Jun 14. doi: 10.1111/cmi.12869.
Flannagan RS, Heit B, and Heinrichs DE. 2016. Intracellular replication of Staphylococcus aureus in mature phagolysosomes in macrophages precedes host cell death, and bacterial escape and dissemination. Cellular Microbiology. 18: 514-535.