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Brucella  are facultative intracellular Gram-negative coccobacilli that chronically infect humans as well as domestic and wild-type mammals, and cause brucellosis. Alternatively activated macrophages (M2a) induced by IL-4/IL-13 via STAT6 signaling pathways have been frequently described as a favorable niche for long-term persistence of intracellular pathogens. Based on the observation that M2a-like macrophages are induced in the spleen during the chronic phase of  B .  abortus  infection in mice and are strongly infected  in vitro , it has been suggested that M2a macrophages could be a potential  in vivo  niche for  Brucella . In order to test this hypothesis, we used a model in which infected cells can be observed directly  in situ  and where the differentiation of M2a macrophages is favored by the absence of an IL-12-dependent Th1 response. We performed an  in situ  analysis by fluorescent microscopy of the phenotype of  B .  melitensis  infected spleen cells from intranasally infected IL-12p40 -/-  BALB/c mice and the impact of STAT6 deficiency on this phenotype. Most of the infected spleen cells contained high levels of lipids and expressed CD11c and CD205 dendritic cell markers and Arginase1, but were negative for the M2a markers Fizz1 or CD301. Furthermore, STAT6 deficiency had no effect on bacterial growth or the reservoir cell phenotype  in vivo , leading us to conclude that, in our model, the infected cells were not Th2-induced M2a macrophages. This characterization of  B .  melitensis  reservoir cells could provide a better understanding of  Brucella  persistence in the host and lead to the design of more efficient therapeutic strategies.

In Situ Characterization of Splenic Brucella melitensis Reservoir Cells during the Chronic Phase of Infection in Susceptible Mice