Study Shows Helminth Infection May Protect Against Obesity Through Immune Protein RELMa
A new mouse study found that transient infection with the helminth parasite Nippostrongylus brasiliensis protected against western diet-induced obesity, with protection dependent on the immunoregulatory protein RELMα. Mice infected with the parasite — which clears naturally within two weeks — showed reduced weight gain, improved glucose tolerance, and less adipocyte enlargement compared to uninfected controls, but these benefits disappeared in mice lacking RELMα. The findings suggest a potential therapeutic target for obesity by harnessing the immune pathways activated during helminth infection.
Researchers using a mouse model of western diet-induced obesity found that a brief infection with the helminth Nippostrongylus brasiliensis conferred lasting metabolic protection, even after the parasite was expelled. Wild-type mice showed attenuated weight gain and improved glucose tolerance, while RELMα knockout mice received no such benefit, establishing RELMα as a critical mediator of this protection. Bulk RNA sequencing of adipose tissue revealed that RELMα promoted enrichment of eosinophils and M2 macrophages — both associated with anti-inflammatory responses — and upregulated pathways linked to fatty acid oxidation, mitochondrial function, and thermogenesis. In contrast, RELMα-deficient mice displayed pro-inflammatory, fibrotic, and lipid-accumulation transcriptional profiles, with changes in collagen and serpin genes confirmed by immunofluorescent staining. The study positions RELMα-driven adipose tissue reprogramming as a promising avenue for developing obesity therapies that target immune dysfunction rather than metabolism directly. The work is currently a preprint on bioRxiv and has not yet undergone peer review.
What's missing
The study is a preprint and has not yet been peer-reviewed. Key open questions include whether these findings translate to humans, given that human helminth infections differ substantially from the mouse model used; whether the protective effects scale with different levels of dietary fat or obesity severity; and what the precise molecular mechanism by which RELMα drives eosinophil and M2 macrophage enrichment is. The study also does not address potential risks or side effects of helminth-based therapeutic strategies in humans.
What different sources said
- bioRxivCenter
Helminth infection induces RELMa-dependent adipose tissue transcriptional reprogramming and protection against diet-induced obesity
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