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Science and Research Wormswell. helminthic therapy, …
Extending the hygiene hypothesis
Although the preponderance of work regarding the relevance of helminth infection and products to diabetes has focused on suppression or regulation of the autoimmune processes underlying T1D, emerging evidence suggests that the ancient relationship between mammals and helminth parasites may also have shaped aspects of metabolism more broadly.
Recent studies in the context of animal models of obesity, metabolic syndrome, and type 2 diabetes have highlighted the contributions of adipose-resident immune populations to the modulation of insulin responsiveness and glucose homeostasis.
Furthermore, as a spontaneous model of autoimmunity, the NOD mouse has enabled detailed exploration of multiple mechanisms by which helminth infections and products exert their influences on underlying autoimmune processes.
Given this long history of basic insight derived from the NOD mouse, it is perhaps surprising that investigation of the hygiene hypothesis in other models of autoimmunity, including those of IBD and MS, have been more rapidly translated to the clinical setting.
Trichuris trichiura - Wikipedia
Infection with the helminth, , was shown to expand the number of both eosinophils and alternatively activated macrophages resident in metabolically active adipose tissue, and to combat insulin resistance in mice fed a high fat diet .
These observations broaden the hygiene hypothesis, suggesting that helminth-derived therapies may have utility in the context of T2D and metabolic syndrome.
As a Th1-mediated disease, it was hypothesized that skewing of the immune response along opposing Th2 and regulatory axes may act to regulate and suppress the diabetogenic Th1 response.
Most of the early papers, showing that helminth infection could prevent diabetes in NOD mice, focused on immune switch from Th1 to Th2 response, and suggested this as the primary mechanism of protection (see Table ).
Kruskal–Wallis test - Handbook of Biological Statistics
sigmodontis; see Table ), and all were found to prevent diabetes, strongly supporting the hypothesis that the immunomodulation induced by helminths has a broad capacity to suppress the onset and progression of T1D [45, 46, 60].
These encouraging findings in the context of live helminth infections led researchers to explore whether soluble antigens from multiple helminth species, in the absence of live infection, also were capable of modulating the initiation and course of autoimmune diabetes in the NOD mouse.
Consistent with the age of this relationship, there is strong evidence that our parasitic passengers have evolved extensive adaptations to life inside the mammalian and, specifically, the human host, and that we, too, have evolved against the backdrop of exposure to helminths and other parasites.
One illustration of this intricate co-evolution can be found in the life cycle of the human blood fluke, Schistosoma mansoni, which is the focus of much of our own work directed at investigation of the hygiene hypothesis in the context of T1D.
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