Abstract
Trypanosomosis is a chronic parasitic infection, affecting both humans and livestock. A common hallmark of experimental murine infections is the occurrence of inflammation and the associated remodelling of the spleen compartment. The latter involves the depletion of several lymphocyte populations, the induction of T‐cell‐mediated immune suppression, and the activation of monocyte/macrophage cell populations. Here, we show that in experimental T b brucei infections in mice, these changes are accompanied by the alteration of the spleen neutrophil compartment. Indeed, mature neutrophils are rapidly recruited to the spleen, and cell numbers remain elevated during the entire infection. Following the second peak of parasitemia, the neutrophil cell influx coincides with the rapid reduction of splenic marginal zone (MZ)B and follicular (Fo)B cells, as well as CD8+ T and NK1.1+ cells, the latter encompassing both natural killer (NK) and natural killer T (NKT) cells. This report is the first to show a comprehensive overview of all alterations in spleen cell populations, measured with short intervals throughout the entire course of an experimental T b brucei infection. These data provide new insights into the dynamic interlinked changes in spleen cell numbers associated with trypanosomosis‐associated immunopathology.
Highlights
Trypanosoma brucei is one of the causative agents of African Trypanosomosis.[1]
Trypanosomosis‐associated immunopathology is linked to excessive activation of the monocyte/macrophage compartment,[5,6,7,8] and results in T‐cell‐mediated immune suppression 9,10 as well as the depletion of several host lymphocyte populations.[5,9,11,12,13]
The neutrophil cell number remains high throughout the progressing infection, reaching a 15‐fold increase following the control of the third peak of infection
Summary
Trypanosoma brucei is one of the causative agents of African Trypanosomosis.[1]. These parasites are continuously exposed to attacks by host antibodies, type 1 proinflammatory cytokines and nitric oxide (NO).[2,3,4] In combination, these molecules can have both direct and indirect trypanotoxic activities. Trypanosomosis‐associated immunopathology is linked to excessive activation of the monocyte/macrophage compartment,[5,6,7,8] and results in T‐cell‐mediated immune suppression 9,10 as well as the depletion of several host lymphocyte populations.[5,9,11,12,13] The latter has been addressed at very specific time points of infection, but so far, comprehensive data detailing with the quantitative dynamic changes of these populations throughout infection is lacking. Upon arrival at the site of inflammation, neutrophils engage their effector functions by eliminating invading pathogens and trigger inflammatory reactions.[14,15,16] recent data demonstrate that neutrophils can extend their functions beyond their role in pathogen clearance and can play a role in promoting parasite survival, in particular, during the onset of tsetse‐transmitted trypanosomosis.[17] The lack of systematic data on quantitative changes in spleen cell numbers throughout infection prompted the data collection reported here
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