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Epigenitic regular on effect of Hpb-colonized and -trained mice on peritoneal macrophage

ABSTRACT: Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.

ORGANISM(S): Mus musculus

PROVIDER: GSE301337 | GEO | 2026/01/01

REPOSITORIES: GEO

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effect of Hpb-colonized and -trained mice on peritoneal macrophage gene expression

Project description:Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.

2026-01-01 | GSE301338 | GEO

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effect of Hpb-colonized and -trained mice on peritoneal macrophage gene expression

Project description:effect of Hpb-colonized and -trained mice on peritoneal macrophage gene expression

| PRJNA1284816 | ENA

Epigenitic regular on effect of Hpb-colonized and -trained mice on peritoneal macrophage

Project description:Epigenitic regular on effect of Hpb-colonized and -trained mice on peritoneal macrophage

| PRJNA1284817 | ENA

Macrophage-regulatory T cell interactions promote type 2 immune homeostasis through Resistin-like molecule α

Project description:RELMα is a small, secreted protein expressed by T helper type 2 (Th2) cytokine activated “M2” macrophages in helminth infection and allergy. At steady state and in response to Th2 cytokines, RELMα is highly expressed by peritoneal macrophages. We generated RELMα TdTomato (Td) reporter/knockout (RΕLMαTd/Td) mice. RELMαTd/Td mice had increased IL-4 induced peritoneal macrophage responses and splenomegaly compared to RELMα+/+ mice. Nanostring data indicated that RELMαTd/Td peritoneal macrophages were more proliferative and activated than RELMα+/+ macrophages, with increased genes associated with T cell response, growth factor and cytokine signaling, but decreased genes associated with differentiation and maintenance of myeloid cells.This studies identify a new RELMα regulatory pathway whereby RELMα-expressing macrophages directly sustain Treg proliferation to limit Th2 inflammatory responses.

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