“…There is a growing body of evidence from animal research supporting the hypothesis that specific helminth infections protect against metabolic disease. Mouse studies have shown that experimental infection with helminths can result in reduced fasting glucose concentrations, decreased fasting insulin concentrations, improved glucose and insulin tolerance, and less insulin resistance in comparison to non-infected controls [25][26][27][28][29].…”
This review has shown that helminth infections can be associated with improved metabolic outcomes. Understanding of the mechanisms underlying this relationship could facilitate the development of novel strategies to prevent or delay T2DM.
“…There is a growing body of evidence from animal research supporting the hypothesis that specific helminth infections protect against metabolic disease. Mouse studies have shown that experimental infection with helminths can result in reduced fasting glucose concentrations, decreased fasting insulin concentrations, improved glucose and insulin tolerance, and less insulin resistance in comparison to non-infected controls [25][26][27][28][29].…”
This review has shown that helminth infections can be associated with improved metabolic outcomes. Understanding of the mechanisms underlying this relationship could facilitate the development of novel strategies to prevent or delay T2DM.
“…Therefore, the role of AAMs in obesity has been studied in the context of helminth infection. Using an experimental model of obese mice infected with T. spiralis , the induction of AAMs triggered by helminth infection led to decreased glucose intolerance and consequent lowering of the blood glucose levels which was associated with AAM markers such as Arg-1, CD206, and IL-10, as well as adipocyte death [69]. These results suggest that AAMs, which are induced by T. spiralis infection, have a beneficial role during obesity through the regulation of the inflammatory process in adipose tissue.…”
Section: Role Of Macrophages During Tissue Migrating and Resident mentioning
The Th1/Th2/Th17 balance is a fundamental feature in the regulation of the inflammatory microenvironment during helminth infections, and an imbalance in this paradigm greatly contributes to inflammatory disorders. In some cases of helminthiasis, an initial Th1 response could occur during the early phases of infection (acute), followed by a Th2 response that prevails in chronic infections. During the late phase of infection, alternatively activated macrophages (AAMs) are important to counteract the inflammation caused by the Th1/Th17 response and larval migration, limiting damage and repairing the tissue affected. Macrophages are the archetype of phagocytic cells, with the primary role of pathogen destruction and antigen presentation. Nevertheless, other subtypes of macrophages have been described with important roles in tissue repair and immune regulation. These types of macrophages challenge the classical view of macrophages activated by an inflammatory response. The role of these subtypes of macrophages during helminthiasis is a controversial topic in immunoparasitology. Here, we analyze some of the studies regarding the role of AAMs in tissue repair during the tissue migration of helminths.
“…M2 macrophages have been implicated in fighting parasitic infections 1 7 and attenuating excessive inflammation 8 , while contributing to tissue remodelling and repair 2 9 . Additionally, M2 macrophages have a central role in regulating glucose tolerance and systemic metabolism 10 11 . Through the release of IL-10, M2 macrophages maintain insulin sensitivity in adipocytes 12 13 and sustain adaptive thermogenesis by inducing thermogenic gene expression in the adipose tissue of mice exposed to cold 14 .…”
Alternatively activated macrophages (M2) have an important function in innate immune responses to parasitic helminths, and emerging evidence also indicates these cells are regulators of systemic metabolism. Here we show a critical role for mTORC2 signalling in the generation of M2 macrophages. Abrogation of mTORC2 signalling in macrophages by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classically activated macrophages (M1) intact. Selective deletion of Rictor in macrophages prevents M2 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the ability of mice to regulate brown fat and maintain core body temperature. Our findings define a role for mTORC2 in macrophages in integrating signals from the immune microenvironment to promote innate type 2 immunity, and also to integrate systemic metabolic and thermogenic responses.
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