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dc.contributor.authorKhudhair, Zainab
dc.contributor.authorAlhallaf, Rafid
dc.contributor.authorEichenberger, Ramon M
dc.contributor.authorWhan, Jen
dc.contributor.authorKupz, Andreas
dc.contributor.authorField, Matt
dc.contributor.authorKrause, Lutz
dc.contributor.authorWilson, David T
dc.contributor.authorDaly, Norelle L
dc.contributor.authorGiacomin, Paul
dc.contributor.authorSotillo, Javier 
dc.contributor.authorLoukas, Alex
dc.date.accessioned2021-03-09T09:54:28Z
dc.date.available2021-03-09T09:54:28Z
dc.date.issued2020
dc.identifier.citationFront Endocrinol (Lausanne). 2021 Feb 5;11:606530.es_ES
dc.identifier.issn1664-2392es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12160
dc.description.abstractType 2 diabetes (T2D) is a major health problem and is considered one of the top 10 diseases leading to death globally. T2D has been widely associated with systemic and local inflammatory responses and with alterations in the gut microbiota. Microorganisms, including parasitic worms and gut microbes have exquisitely co-evolved with their hosts to establish an immunological interaction that is essential for the formation and maintenance of a balanced immune system, including suppression of excessive inflammation. Herein we show that both prophylactic and therapeutic infection of mice with the parasitic hookworm-like nematode, Nippostrongylus brasiliensis, significantly reduced fasting blood glucose, oral glucose tolerance and body weight gain in two different diet-induced mouse models of T2D. Helminth infection was associated with elevated type 2 immune responses including increased eosinophil numbers in the mesenteric lymph nodes, liver and adipose tissues, as well as increased expression of IL-4 and alternatively activated macrophage marker genes in adipose tissue, liver and gut. N. brasiliensis infection was also associated with significant compositional changes in the gut microbiota at both the phylum and order levels. Our findings show that N. brasiliensis infection drives changes in local and systemic immune cell populations, and that these changes are associated with a reduction in systemic and local inflammation and compositional changes in the gut microbiota which cumulatively might be responsible for the improved insulin sensitivity observed in infected mice. Our findings indicate that carefully controlled therapeutic hookworm infection in humans could be a novel approach for treating metabolic syndrome and thereby preventing T2D.es_ES
dc.description.sponsorshipThis work was supported by the National Health and Medical Research Council (NHMRC) through a program grant (1132975) and senior principal research fellowship (1117504) to AL, an AITHM Capacity Building grant to PG, AL, and MF, and an Australian Research Council Special Research Initiative award to the Australian Institute of Tropical Health and Medicine at James Cook University (SRI40200003). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectM2 macrophageses_ES
dc.subjectNippostrongylus brasiliensises_ES
dc.subjectEosinophilses_ES
dc.subjectHelminthes_ES
dc.subjectHigh fat dietes_ES
dc.subjectHigh glycemic index dietes_ES
dc.subjectMicrobiotaes_ES
dc.subjectType 2 diabeteses_ES
dc.titleGastrointestinal helminth infection improves insulin sensitivity, decreases systemic inflammation, and alters the composition of gut microbiota in distinct mouse models of Type 2 Diabeteses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33613446es_ES
dc.format.volume11es_ES
dc.format.page606530es_ES
dc.identifier.doi10.3389/fendo.2020.606530es_ES
dc.contributor.funderNational Health and Medical Research Council (Australia) 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fendo.2020.606530es_ES
dc.identifier.journalFrontiers in endocrinologyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución 4.0 Internacional