In vivo reduction of Treg expansion in rodent helminth–malaria coinfection
Abstract
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.
Related
- Monocyte regulatory phenotypes and systemic proteomic signatures in helminth-tuberculosis coinfection
- Coinfection of Two Endemics – Scrub Typhus and Malaria
- Liver-Resident Metabolic Reprogramming and Th2/1 Cell Accumulation Drive Anti-Helminth Immunity During H. bakeri InfectionRunning title: Liver metabolic-immune crosstalk in helminth infection
- Staphylococcus aureus coagulases increase survival of Pseudomonas aeruginosa during coinfection
- RSV & rhinovirus coinfection order dictates outcome via type III interferon-mediated interference in infant respiratory epithelium
BibTeX
@article{bourbon2026vivo,
title = {{In vivo reduction of Treg expansion in rodent helminth–malaria coinfection}},
author = {Luc Bourbon and Aloïs Dusuel and Nicolas Pernet and Mickaël Rialland and Benjamin Roche and Bruno Faivre and Gabriele Sorci},
journal = {Parasites \& Vectors},
year = {2026},
month = jun,
doi = {10.1186/s13071-026-07465-3},
url = {https://hal.science/hal-05847907v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - In vivo reduction of Treg expansion in rodent helminth–malaria coinfection
AU - Luc Bourbon
AU - Aloïs Dusuel
AU - Nicolas Pernet
AU - Mickaël Rialland
AU - Benjamin Roche
AU - Bruno Faivre
AU - Gabriele Sorci
PY - 2026
DA - 2026/06/13
JO - Parasites & Vectors
DO - 10.1186/s13071-026-07465-3
UR - https://hal.science/hal-05847907v1
AB - 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.
SN - 1756-3305
SN - 1756-3305
ER -