Abstract
Neutrophils (PMNs) are the first line of defense against bacteria entering the body. However, it has been shown that Brucella induce low PMN activation and survive within these leukocytes by resisting their microbicidal mechanisms. Brucella also induce the premature cell death of PMNs, which release chemokines and express ‘eat me’ signals. These PMNs are then phagocyted by mononuclear cells where Brucella replicate. This evidence suggests that PMNs may behave as vehicles protecting Brucella from immune recognition, favoring their dispersion to the target organs. To test this hypothesis, we analyzed the course of infection in mice intraperitoneally infected with B. abortus alone (Ba) or with Brucella-infected PMNs (Ba-PMN). We evaluated bacterial loads, histopathological analyzes in selected tissues, cytokine production in serum, anti-Brucella antibody titers, and hematological parameters. We observed that mice infected with Ba-PMN had lower bacterial loads in the spleen and bone marrow at seven days of post-infection compared to Ba. The bacterial load then became equivalent at 30 days post-infection. The pathological index demonstrated a similar trend to the bacterial load. Ba-PMN infected mice showed less granulomatous inflammation in the spleen and bone marrow at seven days post-infection than the Ba group but with similar indexes at day 30. Comparably, Ba-PMN infected mice showed less IFN-gamma and IL-6 at the beginning of the infection than the Ba group but with similar concentrations at the end of the experiment. Ba-PMN infected mice also showed fewer anti-Brucella antibody titers at day 30 than the Ba group. No significant differences were observed between infected groups in the hematological values at 7 or 30 days. Despite both groups reaching similar bacterial loads by day 30, the bacterial loads and the immunological parameter were lower at the beginning of the infection in the Ba-PMN group. We conclude that the course of infection in the Ba-PMN group was stealthier than in the Ba group. Despite the slower course of Brucella infection in the Ba-PMN, PMNs supported their dispersion to a similar extent but with reduced immune recognition.
