| Literature DB >> 35787830 |
Sara Silva Pereira1, Mariana De Niz1, Karine Serre1, Marie Ouarné1, Joana E Coelho1, Cláudio A Franco1, Luisa M Figueiredo1.
Abstract
Trypanosoma congolense causes a syndrome of variable severity in animals in Africa. Cerebral trypanosomiasis is a severe form, but the mechanism underlying this severity remains unknown. We developed a mouse model of acute cerebral trypanosomiasis and characterized the cellular, behavioral, and physiological consequences of this infection. We show large parasite sequestration in the brain vasculature for long periods of time (up to 8 hr) and extensive neuropathology that associate with ICAM1-mediated recruitment and accumulation of T cells in the brain parenchyma. Antibody-mediated ICAM1 blocking and lymphocyte absence reduce parasite sequestration in the brain and prevent the onset of cerebral trypanosomiasis. Here, we establish a mouse model of acute cerebral trypanosomiasis and we propose a mechanism whereby parasite sequestration, host ICAM1, and CD4+ T cells play a pivotal role.Entities:
Keywords: Trypanosoma congolense; cerebral trypanosomiasis; infectious disease; microbiology; nagana; sequestration; virulence
Mesh:
Year: 2022 PMID: 35787830 PMCID: PMC9307270 DOI: 10.7554/eLife.77440
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.713