Parasites & vectors · 2026
In vivo reduction of Treg expansion in rodent helminth-malaria coinfection.
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Bourbon Luc, Dusuel Aloïs, Pernet Nicolas, Rialland Mickaël, Roche Benjamin, Faivre Bruno, Sorci Gabriele
Аннотация
BACKGROUND: Parasitic helminths modulate host immunity to establish chronic infections, often expanding regulatory T cells (Tregs) to suppress inflammation. However, how helminths adjust immunomodulation during coinfection with fast-replicating microparasites remains unclear. Here, we investigated the immune modulation dynamics in a murine model coinfected with the nematode Heligmosomoides polygyrus (Hp) and the protozoan Plasmodium yoelii (Py).
METHODS: We compared Treg expansion in single Hp infected and coinfected mice, assessed Hp excretory-secretory products (HES) for Treg induction in vitro, measured expression of the TGF-β mimic Hp-TGM-1 gene, and conducted experimental evolution over eight generations in single and coinfected hosts.
RESULTS: Although coinfected mice exhibited reduced Treg expansion in vivo, HES collected from worms in single infected and coinfected hosts induced similar Treg expansion in vitro. Furthermore, Hp-TGM-1 expression was found to be upregulated in worms from coinfected hosts. Experimental evolution revealed no consistent differences between Hp lines (i.e., parasites maintained in single infected or coinfected hosts).
CONCLUSIONS: These results suggest that reduced Treg expansion during coinfection is driven by the host rather than the parasite, which informs our understanding of immune modulation in helminth-malaria coinfections.
METHODS: We compared Treg expansion in single Hp infected and coinfected mice, assessed Hp excretory-secretory products (HES) for Treg induction in vitro, measured expression of the TGF-β mimic Hp-TGM-1 gene, and conducted experimental evolution over eight generations in single and coinfected hosts.
RESULTS: Although coinfected mice exhibited reduced Treg expansion in vivo, HES collected from worms in single infected and coinfected hosts induced similar Treg expansion in vitro. Furthermore, Hp-TGM-1 expression was found to be upregulated in worms from coinfected hosts. Experimental evolution revealed no consistent differences between Hp lines (i.e., parasites maintained in single infected or coinfected hosts).
CONCLUSIONS: These results suggest that reduced Treg expansion during coinfection is driven by the host rather than the parasite, which informs our understanding of immune modulation in helminth-malaria coinfections.