Trypanosoma brucei Infection Directly Infiltrates Female Reproductive Tract and Disrupts Reproductive Function Through Immune and Hormonal Pathways
A new murine study published on bioRxiv shows that Trypanosoma brucei, the parasite causing Human African Trypanosomiasis (sleeping sickness), directly infiltrates the uterine lining and triggers widespread reproductive dysfunction. Researchers found that both acute and chronic infection remodel the uterine immune environment, disrupt the hormonal axis governing reproduction, and cause ovarian atrophy and follicular degeneration. The findings suggest that reproductive pathology in sleeping sickness involves distinct immune and endocrine mechanisms, with implications for how systemic parasitic infections are studied more broadly.
Researchers using a mouse model of Trypanosoma brucei infection have demonstrated for the first time that the parasite directly localizes within the endometrium (uterine lining) during both acute and chronic infection stages. Chronic infection was associated with fat wasting, disruption of the oestrous cycle, uterine and ovarian atrophy, and extensive transcriptional dysregulation along the hypothalamic-pituitary-gonadal (HPG) axis — the hormonal cascade that governs reproduction. Immune profiling revealed significant remodelling of the uterine immune landscape, including T cell infiltration, pro-inflammatory myeloid activation, and broader type 1 inflammatory changes across reproductive tissues. Ovarian pathology included follicular degeneration, reduced corpora lutea, and alterations to steroidogenic (hormone-producing) pathways. Notably, hormonal rescue using tamoxifen, a selective oestrogen receptor modulator, restored uterine morphology and prevented oestrous cycle arrest but failed to reverse infection-driven immune remodelling, indicating that endocrine dysfunction and inflammation operate through separate pathways. The study, currently a preprint and not yet peer-reviewed, calls for the female reproductive tract to be more systematically assessed in other models of systemic inflammation.
What's missing
As a preprint, this study has not yet undergone formal peer review, and its findings are based solely on a murine model; direct evidence of these mechanisms in human T. brucei infection is lacking. The study does not address whether male reproductive tracts are similarly affected, nor does it examine whether the observed pathology is reversible upon parasite clearance. The generalizability of tamoxifen as a potential therapeutic intervention in humans with HAT remains entirely unexplored.
What different sources said
- bioRxivCenter
Trypanosoma brucei infection remodels the uterine immune environment and drives neuroendocrine dysfunction
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