Transfer of immunity to<i>Trichinella spiralis</i>in the mouse with mesenteric lymph node cells: time of appearance of effective cells in donors and expression of immunity in recipients

Wakelin, D.; Wilson, Margaret M.

doi:10.1017/s0031182000047843

Cited by 77 publications

(41 citation statements)

References 13 publications

(13 reference statements)

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“…The methods used for infecting mice and recovering T. spiralis worms were as described previously (Wakelin and Wilson 1977). FOLIA PARASITOLOGICA 47: 55-59, 2000 Male C57BL mice, aged 10-14 weeks, obtained from "Ruđer Bošković" Institute, Zagreb, Croatia, were infected with 200 T. spiralis infective muscle larvae (L1) on day 0.…”

Section: Methodsmentioning

confidence: 99%

Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Božić¹,

Tran²,

E³

2000

FOLIA PARASIT

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Abstract. The potential role of intestinal intraepithelial lymphocytes (i-IELs) in the generation of host protective immunity after helminth infection was investigated using the Trichinella spiralis (Owen, 1835)/mouse model. In this study we found a significant rise of TCRγδ + i-IELs (P < 0.001) concurrent with the jejunal goblet cells (GC) hyperplasia in T. spiralis-infected C57BL mice on day 4 p.i. However, no direct relationship between the kinetics of the increase in TCRγδ + i-IELs and T. spiralis expulsion was observed in infected mice. Taken together, these results implicate that γδ i-IELs probably perform a unique functions related to the regulation of the GC proliferation accompanying T. spiralis gut infection. As is known, these TCRγδ + i-IELs may release mediators or growth factors that in turn influence GC differentiation. With the use of dexamethason (DEX), a potent anti-inflammatory agent which also induces apoptotic cell death in i-IELs, we have confirmed that the expulsion of T. spiralis from the mouse gut is accompanied by an inflammatory response. Indeed, the GC are clearly involved in these phenomena, apparently under the regulation by TCRγδ + i-IEL-mediated responses, since DEX abrogated GC proliferation in T. spiralis-infected C57BL mice and subsequently augmented adult worm burden. Our data also show that the rejection of adult worms starts concurrently with a significant increase in TCRαβ + and CD8 + i-IELs (P < 0.05 and P ≤ 0.01, respectively), namely by day 7 p.i. At the same time, CD4+ cells significantly decreased (P < 0.05) in the intestinal epithelium of T. spiralis-infected, vs uninfected mice. These results may indicate that the TCRαβ + and CD8 + i-IELs act as effectors of anti-T. spiralis defence reactions. The implications of these findings for the potential role of intestinal intraepithelial CD8 + and TCRαβ + cells in the pathogenesis of the intestinal lesions during T. spiralis gut infection are discussed.

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Section: Methodsmentioning

confidence: 99%

Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Božić¹,

Tran²,

E³

2000

FOLIA PARASIT

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“…Maintenance, infection, and recovery of T. spiralis larvae was based on standard methods (16). Sex-matched 8-to 15-wk-old BALB/c or C57BL/10 mice were infected by gavage with 200 -300 muscle larvae per mouse in 0.2 ml of PBS/0.1% agar.…”

Section: Parasite Infections and Tissue Preparationmentioning

confidence: 99%

Innate BALB/c Enteric Epithelial Responses to Trichinella spiralis: Inducible Expression of a Novel Goblet Cell Lectin, Intelectin-2, and Its Natural Deletion in C57BL/10 Mice

Pemberton

Knight

Gamble

et al. 2004

The Journal of Immunology

121

132

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Infection of mice with the nematode parasite Trichinella spiralis induces changes in the proteome of the jejunal epithelium, including substantial up-regulation of a novel variant of interlectin. In this study we sequence this novel lectin, termed intelectin-2, and compare expression levels during T. spiralis infection of resistant (BALB/c) with susceptible (C57BL/10) mouse strains. Intelectin-2 was cloned and sequenced from BALB/c mRNA extracted on day 14 of infection, and was found to have 91% amino acid identity with intelectin (within our study termed intelectin-1). Intelectin-2 transcripts were up-regulated early (day 3) during infection with T. spiralis in BALB/c mice, suggesting an innate response, and levels remained high through to day 14 (time of parasite rejection). Immunohistochemistry of jejunal sections with a rabbit polyclonal Ab to Xenopus laevis 35-kDa cortical granule lectin (XL35; 68% identity with intelectin-2) followed a similar pattern, with intense labeling of goblet and Paneth cells at day 14. However, intelectin-2 transcripts and protein were absent, and immunohistochemistry negative when C57BL/10 mice were infected with T. spiralis. Genomic PCR and Southern blotting confirmed that the intelectin-2 gene is absent from the C57BL/10 genome. The presence of intelectin-2 in resistant BALB/c mice, its absence from the susceptible C57BL/10 strain and the kinetics of its up-regulation during T. spiralis infection suggest that this novel lectin may serve a protective role in the innate immune response to parasite infection.

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“…Mice were infected with T. spiralis at 6 -8 wk of age. Maintenance, infection, and recovery of T. spiralis were as previously described (31). Mice were infected by oral gavage with 300 larvae on day 0.…”

Section: Animals and Infectionmentioning

confidence: 99%

Intraepithelial NK Cell-Derived IL-13 Induces Intestinal Pathology Associated with Nematode Infection

McDermott

Humphreys

Forman

et al. 2005

The Journal of Immunology

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IL-13 is a Th2-derived cytokine associated with pathological changes in asthma and ulcerative colitis. Moreover, it plays a major role in the control of gut nematode infection and associated immunopathology. The current paradigm is that these effects are due to T cell-derived IL-13. We show in this study that an innate source of IL-13, the intraepithelial NK cell, is responsible for the disruption of intestinal tissue architecture and induction of goblet cell hyperplasia that characterizes infection with the intestinal helminth Trichinella spiralis. IL-13 or IL-4Rα (but not IL-4) null mice failed to induce intestinal pathology. Unexpectedly, SCID and athymic mice developed the same pathology found in immunocompetent mice following infection. Moreover, immunodeficient mice expressed IL-13 in the intestine, and abnormal mucosal pathology was reduced by in vivo administration of a soluble IL-13 antagonist. IL-13 expression was induced in non-T intraepithelial CD3− NK cells. Epithelial cells expressed the IL-13 signaling receptor, IL-13Rα1, and after infection, IL-4Rα. Furthermore, the soluble IL-13 decoy receptor IL-13Rα2, which regulates IL-13 responses, was also induced upon infection. These data provide the first evidence that intestinal tissue restructuring during helminth infection is an innate event dependent on IL-13 production by NK cells resident in the epithelium of the intestine.

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Transfer of immunity toTrichinella spiralisin the mouse with mesenteric lymph node cells: time of appearance of effective cells in donors and expression of immunity in recipients

Cited by 77 publications

References 13 publications

Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Innate BALB/c Enteric Epithelial Responses to Trichinella spiralis: Inducible Expression of a Novel Goblet Cell Lectin, Intelectin-2, and Its Natural Deletion in C57BL/10 Mice

Intraepithelial NK Cell-Derived IL-13 Induces Intestinal Pathology Associated with Nematode Infection

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