Coinfection with
 Heligmosomoides polygyrus
 Fails To Establish CD8
 +
 T-Cell Immunity against
 Toxoplasma gondii

Khan, Imtiaz Ali; Hakak, Rubeena; Eberle, Karen E.; Sayles, Peter C.; Weiss, Louis M.; Urban, Joseph F.

doi:10.1128/iai.00277-08

Cited by 10 publications

(12 citation statements)

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“…Such an effect of nematodes with relatively little intrinsic pathogenicity appears to be beneficial for the host and is currently being explored as a therapeutic means to control inflammatory bowel disease in humans (63) and possibly other autoimmune diseases (37). On the other hand, the helminths may be detrimental under conditions in which a strong proinflammatory response is necessary to control other infectious agents (20,29,33,39,66).…”

Section: Discussionmentioning

confidence: 99%

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

et al. 2008

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Infection with the trematode helminth Schistosoma mansoni results in a parasite egg-induced, CD4 T-cellmediated, hepatointestinal granulomatous and fibrosing inflammation that varies greatly in severity, with a higher frequency of milder forms typically occurring in regions where the disease is endemic. One possible explanation for this is that in these regions the degree of inflammation is lessened by widespread concurrent infection with gastrointestinal nematodes. We tested this hypothesis by establishing a murine coinfection model in which mice were infected with the intestinal nematode parasite Heligmosomoides polygyrus prior to infection with S. mansoni. In CBA mice that naturally display a severe form of schistosomiasis, preinfection with H. polygyrus resulted in a marked reduction in schistosome egg-induced hepatic immunopathology, which was associated with significant decreases in the levels of interleukin-17 (IL-17), gamma interferon, tumor necrosis factor alpha, IL-23, IL-6, and IL-1␤ and with increases in the levels of IL-4, IL-5, IL-10, and transforming growth factor ␤ in mesenteric lymph node cells, purified CD4 T cells, and isolated liver granuloma cells. There also were increases in liver Ym1 and forkhead box P3 transcription factor expression. In another model of high-pathology schistosomiasis induced in C57BL/6 mice by immunization with schistosome egg antigens in complete Freund's adjuvant, coinfection with the nematodes also resulted in a marked inhibition of hepatic immunopathology accompanied by similar shifts in cytokine production. These findings demonstrate that intestinal nematodes prevent Th1-and Th17-cell-mediated inflammation by promoting a strong Th2-polarized environment associated with increases in the levels of alternatively activated macrophages and T regulatory cells, which result in significant amelioration of schistosome-induced immunopathology.

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Section: Discussionmentioning

confidence: 99%

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

et al. 2008

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“…These observations provide strong evidence to demonstrate that helminth infection can dampen Th1 reactions to other infections and cause impaired immune responses to concurrent viral, bacterial, and parasite infections, as well as to vaccination. The Th2-inducing helminth infection has also been shown to inhibit the development of CD8+ T cell responses [43] .…”

Section: Helminths Affect Host Responses To Other Antigens and Pathogensmentioning

confidence: 99%

Helminth infections and intestinal inflammation

Wang

Cao²,

Shi³

2008

WJG

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“…In this way H. bakeri could facilitate its own survival for extraordinarily long periods in mouse strains otherwise totally competent immunologically (Behnke et al 1983 ;Behnke, 1987), a strategy now known to be utilized by many other nematodes and other helminths that cause longlasting chronic infections Maizels et al 2004). Even strains having the capacity to generate a potent mastocytosis in response to infection with T. spiralis, failed to do so when they harboured H. bakeri (Dehlawi et al 1987 ;Dehlawi and Wakelin, 1988) and the generation of both CD8+ and CD4+ T cells to heterologous infections was greatly suppressed (Khan et al 2008). This immunosuppressive effect allowed other species of parasites, which normally would have been expelled, to survive for much longer periods in concurrently infected mice (Colwell and Wescott, 1973 ;Courtney and Forrester, 1973 ;Della Bruna and Xenia, 1976 ;Behnke et al 2001).…”

Section: G E N E T I C S O F T H E H O S T R E S P O N S E T O C H R mentioning

confidence: 99%

Heligmosomoides bakeri: a model for exploring the biology and genetics of resistance to chronic gastrointestinal nematode infections

2009

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A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription. The intestinal nematode Heligmosomoides bakeri has undergone 2 name changes during the last 4 decades. Originally, the name conferred on the organism in the early 20th century was Nematospiroides dubius, but this was dropped in favour of Heligmosomoides polygyrus, and then more recently H. bakeri, to distinguish it from a closely related parasite commonly found in wood mice in Europe. H. bakeri typically causes long-lasting infections in mice and in this respect it has been an invaluable laboratory model of chronic intestinal nematode infections. Resistance to H. bakeri is a dominant trait and is controlled by genes both within and outside the MHC. More recently, a significant QTL has been identified on chromosome 1, although the identity of the underlying genes is not yet known. Other QTL for resistance traits and for the accompanying immune responses were also defined, indicating that resistance to H. bakeri is a highly polygenic phenomenon. Hence marker-assisted breeding programmes aiming to improve resistance to GI nematodes in breeds of domestic livestock will need to be highly selective, focussing on genes that confer the greatest proportion of overall genetic resistance, whilst leaving livestock well-equipped genetically to cope with other types of pathogens and preserving important production traits.

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Coinfection with Heligmosomoides polygyrus Fails To Establish CD8 ⁺ T-Cell Immunity against Toxoplasma gondii

Cited by 10 publications

References 0 publications

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

Helminth infections and intestinal inflammation

Heligmosomoides bakeri: a model for exploring the biology and genetics of resistance to chronic gastrointestinal nematode infections

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Coinfection with Heligmosomoides polygyrus Fails To Establish CD8 + T-Cell Immunity against Toxoplasma gondii

Cited by 10 publications

References 0 publications

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

Coinfection with the Intestinal NematodeHeligmosomoides polygyrusMarkedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

Helminth infections and intestinal inflammation

Heligmosomoides bakeri: a model for exploring the biology and genetics of resistance to chronic gastrointestinal nematode infections

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Product

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Coinfection with Heligmosomoides polygyrus Fails To Establish CD8 ⁺ T-Cell Immunity against Toxoplasma gondii