Schistosoma Infection and Schistosoma-Derived Products Modulate the Immune Responses Associated with Protection against Type 2 Diabetes

Tang, Chun-lian; Liu, Zhiming; Gao, Yan; Xiong, Fei

doi:10.3389/fimmu.2017.01990

Cited by 18 publications

(12 citation statements)

References 73 publications

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“…Further research is evaluating whether helminth-derived molecules could be developed as novel therapeutic approaches to diabetes and metabolic syndrome. 82 In addition, a prospective randomised-control trial of helminth eradiation by albendazole therapy in Indonesia 83 is underway evaluating the impact of helminth infections on insulin resistance.…”

Section: Diabetes and Specific Infectionsmentioning

confidence: 99%

The double burden of diabetes and global infection in low and middle-income countries

Dunachie

Chamnan

2018

Transactions of the Royal Society of Tropical Medicine and Hygiene

138

106

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Four out of five people in the world with diabetes now live in low- and middle-income countries (LMIC), and the incidence of diabetes is accelerating in poorer communities. Diabetes increases susceptibility to infection and worsens outcomes for some of the world’s major infectious diseases such as tuberculosis, melioidosis and dengue, but the relationship between diabetes and many neglected tropical diseases is yet to be accurately characterised. There is some evidence that chronic viral infections such as hepatitis B and HIV may predispose to the development of type 2 diabetes by chronic inflammatory and immunometabolic mechanisms. Helminth infections such as schistosomiasis may be protective against the development of diabetes, and this finding opens up new territory for discovery of novel therapeutics for the prevention and treatment of diabetes. A greater understanding of the impact of diabetes on risks and outcomes for infections causing significant diseases in LMIC is essential in order to develop vaccines and therapies for the growing number of people with diabetes at risk of infection, and to prioritise research agendas, public health interventions and policy. This review seeks to give an overview of the current international diabetes burden, the evidence for interactions between diabetes and infection, immune mechanisms for the interaction, and potential interventions to tackle the dual burden of diabetes and infection.

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Section: Diabetes and Specific Infectionsmentioning

confidence: 99%

The double burden of diabetes and global infection in low and middle-income countries

Dunachie

Chamnan

2018

Transactions of the Royal Society of Tropical Medicine and Hygiene

138

106

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“…Finally, when investigators evaluated the beneficial impact of helminth on protecting against the development of metabolic disorders, including obesity and dyslipidemia, commonly associated with insulin resistance and type 2 diabetes, parasite‐induced IL‐10 and the type 2 immune responses seem to act to improve insulin sensitivity 116 , thereby ameliorating the metabolic syndrome (MetS)-associated morbidity 117 . In this context, it has been shown that helminths have an important beneficial role by skewing this inflammatory response toward one with IL-4-producing eosinophils, M2 macrophages, and Treg cells that maintain insulin signaling and sensitivity 118 .…”

Section: Helminth Infections and Autoimmune And Metabolic Disordersmentioning

confidence: 99%

Helminth parasites and immune regulation

2018

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Helminth parasites are complex metazoans that belong to different taxonomic families but that collectively share the capacity to downregulate the host immune response directed toward themselves (parasite-specific immunoregulation). During long-standing chronic infection, these helminths appear able to suppress immune responses to bystander pathogens/antigens and atopic, autoimmune, and metabolic disorders. Helminth-induced immunoregulation occurs through the induction of regulatory T cells or Th2-type cells (or both). However, secreted or excreted parasite metabolites, proteins, or extracellular vesicles (or a combination of these) may also directly induce signaling pathways in host cells. Therefore, the focus of this review will be to highlight recent advances in understanding the immune responses to helminth infection, emphasizing the strategies/molecules and some of the mechanisms used by helminth parasites to modulate the immune response of their hosts.

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“…Also, our previous study demonstrated that Trichinella spiralis infection derived T reg cells were the key cells mediating the amelioration of allergic airway inflammation and DSS-induced colitis in mice 35,36 . Infection with parasites such as Brugia malayi and Schistosoma mansoni triggers M2 macrophages 37–41 . A previous study reported that T. spiralis infection induced YM1-expressing M2 macrophages, but the function of these cells remains unclear 42–44 .…”

Section: Introductionmentioning

confidence: 99%

Adoptive transfer of Trichinella spiralis-activated macrophages can ameliorate both Th1- and Th2-activated inflammation in murine models

Kang

Park

et al. 2019

Sci Rep

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Trichinella spiralis is a zoonotic nematode and food borne parasite and infection with T . spiralis leads to suppression of the host immune response and other immunopathologies. Alternative activated macrophages (M2) as well as T reg cells, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite. The precise mechanism by which helminths modulate host immune response is not fully understood. To determine the functions of parasite-induced M2 macrophages, we compared the effects of M1 and M2 macrophages obtained from Trichinella spiralis- infected mice with those of T . spiralis excretory/secretory (ES) protein-treated macrophages on experimental intestinal inflammation and allergic airway inflammation. T . spiralis infection induced M2 macrophage polarization by increasing the expression of CD206, ARG1 , and Fizz2 . In a single application, we introduced macrophages obtained from T . spiralis- infected mice and T . spiralis ES protein-treated macrophages into mice tail veins before the induction of dextran sulfate sodium (DSS)-induced colitis, ovalbumin (OVA)-alum sensitization, and OVA challenge. Colitis severity was assessed by determining the severity of colitis symptoms, colon length, histopathologic parameters, and Th1-related inflammatory cytokine levels. Compared with the DSS-colitis group, T . spiralis- infected mice and T . spiralis ES protein-treated macrophages showed significantly lower disease activity index (DAI) at sacrifice and smaller reductions of body weight and proinflammatory cytokine level. The severity of allergic airway inflammation was assessed by determining the severity of symptoms of inflammation, airway hyperresponsiveness (AHR), differential cell counts, histopathologic parameters, and levels of Th2-related inflammatory cytokines. Severe allergic airway inflammation was induced after OVA-alum sensitization and OVA challenge, which significantly increased Th2-related cytokine levels, eosinophil infiltration, and goblet cell hyperplasia in the lung. However, these severe allergic symptoms were significantly decreased in T. spiralis- infected mice and T. spiralis ES protein-treated macrophages. Helminth infection and helminth ES proteins induce M2 macrophages. Adoptive transfer of macrophages obtained from helminth-infected mice and helminth ES protein-activated macrophages is an effective treatment for preventing and treating airway allergy in mice and is promising as a therapeutic for treating inflammatory diseases.

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Schistosoma Infection and Schistosoma-Derived Products Modulate the Immune Responses Associated with Protection against Type 2 Diabetes

Cited by 18 publications

References 73 publications

The double burden of diabetes and global infection in low and middle-income countries

The double burden of diabetes and global infection in low and middle-income countries

Helminth parasites and immune regulation

Adoptive transfer of Trichinella spiralis-activated macrophages can ameliorate both Th1- and Th2-activated inflammation in murine models

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