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We have previously reported that  Rickettsia conorii  and  Rickettsia montanensis  have distinct intracellular fates within THP-1 macrophages, suggesting that the ability to proliferate within macrophages may be a distinguishable factor between pathogenic and non-pathogenic Spotted fever group (SFG) members. To start unraveling the molecular mechanisms underlying the capacity (or not) of SFG  Rickettsia  to establish their replicative niche in macrophages, we have herein used quantitative proteomics by SWATH-MS to profile the alterations resulted by the challenge of THP-1 macrophages with  R. conorii  and  R. montanensis . We show that the pathogenic,  R. conorii , and the non-pathogenic,  R. montanensis , member of SFG  Rickettsia  trigger differential proteomic signatures in macrophage-like cells upon infection.  R. conorii  specifically induced the accumulation of several enzymes of the tricarboxylic acid cycle, oxidative phosphorylation, fatty acid  β -oxidation, and glutaminolysis, as well as of several inner and outer membrane mitochondrial transporters. These results suggest a profound metabolic rewriting of macrophages by  R. conorii  toward a metabolic signature of an M2-like, anti-inflammatory activation program. Moreover, several subunits forming the proteasome and immunoproteasome are found in lower abundance upon infection with both rickettsial species, which may help bacteria to escape immune surveillance.  R. conorii -infection specifically induced the accumulation of several host proteins implicated in protein processing and quality control in ER, suggesting that this pathogenic  Rickettsia  may be able to increase the ER protein folding capacity. This work reveals novel aspects of macrophage- Rickettsia  interactions, expanding our knowledge of how pathogenic rickettsiae explore host cells to their advantage.

A Pathogen and a Non-pathogen Spotted Fever Group Rickettsia Trigger Differential Proteome Signatures in Macrophages