Differences in Intracellular Fate of Two Spotted Fever Group Rickettsia in Macrophage-Like Cells

Pedro Curto1, Isaura Simões2, Sean P Riley3

  • 1PhD Programme in Experimental Biology and Biomedicine, Center for Neuroscience and Cell Biology, University of CoimbraCoimbra, Portugal; Institute for Interdisciplinary Research, University of CoimbraCoimbra, Portugal; Center for Neuroscience and Cell BiologyCoimbra, Portugal; Vector Borne Disease Laboratories, Department of Pathobiological Sciences, LSU School of Veterinary MedicineBaton Rouge, LA, USA.

Insights

Spotted fever group rickettsiae pathogenesis differs based on macrophage interaction. Pathogenic Rickettsia conorii proliferates in macrophages, unlike non-pathogenic Rickettsia montanensis, explaining disease association differences.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Cell Biology

Background:

  • Spotted fever group (SFG) rickettsiae cause tick-borne diseases globally.
  • Recent evidence suggests non-endothelial cell interactions are key to SFG rickettsiae pathogenesis.
  • The role of macrophages in rickettsial disease pathogenesis may be underestimated.

Purpose of the Study:

  • To investigate the role of macrophages in SFG rickettsiae pathogenesis.
  • To compare the ability of pathogenic Rickettsia conorii and non-virulent Rickettsia montanensis to proliferate in macrophage-like cells and non-phagocytic cells.

Main Methods:

  • In vitro proliferation assays using THP-1 macrophage-like cells and non-phagocytic cell lines.
  • Bacterial association and invasion assays with THP-1 derived macrophages.
  • Co-localization studies using LAMP-2 and cathepsin D markers.

Main Results:

  • Rickettsia conorii survived and proliferated in both phagocytic and epithelial cells.
  • Rickettsia montanensis showed limited proliferation in THP-1 cells, with defective binding and rapid destruction within lysosomes.
  • Rickettsia conorii survived freely in the cytoplasm of both cell types.

Conclusions:

  • A key difference between pathogenic and non-pathogenic SFG rickettsiae lies in their ability to proliferate within macrophages.
  • Macrophage interaction and survival mechanisms may explain the varying disease association of different SFG rickettsial species.