Immunolocalization and pathological alterations following Strongyloides venezuelensis infection in the lungs and the intestine of MHC class I or II deficient mice

Gonçalves, Ana Lúcia Ribeiro; Rodrigues, Raphael Silva; Silva, N.M.; Gonçalves, Flávia A; Cardoso, Cristina Ribeiro de Barros; Beletti, Marcelo Emı́lio; Ueta, Marlene Tiduko; Silva, J.S.; Costa-Cruz, Júlia Maria

doi:10.1016/j.vetpar.2008.09.023

Cited by 12 publications

(17 citation statements)

References 31 publications

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“…We found that T and B cell-deficient Rag2 -/-mice exhibited a 20-day delay (i.e., requiring 32 days in total) in cessation of S. venezuelensis egg excretion during primary infections and a 25-day delay (i.e., requiring 37 days in total) in the secondary infection (versus no eggs detected during secondary infections in any of the wild-type mice) (Fig. 3A), underscoring the importance of an adaptive immune response for effective secondary immune responses to this nematode (8,11,13,14,41,(46)(47)(48). In addition, we confirmed that the number of adult worms in the intestines on day 8 of the primary infection was significantly higher in the Rag2 -/-mice than in the corresponding wild-type mice (Fig.…”

Section: Resultsmentioning

confidence: 84%

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

et al. 2017

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There is evidence that mast cells, basophils, and IgE can contribute to immune responses to parasites; however, the relative levels of importance of these effector elements in parasite immunity are not fully understood. Previous work in Il3-deficient and c-kit mutant Kit W/W-v mice indicated that interleukin-3 and c-Kit contribute to expulsion of the intestinal nematode Strongyloides venezuelensis during primary infection. Our findings in mast cell-deficient Kit W-sh/W-sh mice and two types of mast cell-deficient mice that have normal c-kit ("Hello Kitty" and MasTRECK mice) confirmed prior work in Kit W/W-v mice that suggested that mast cells play an important role in S. venezuelensis egg clearance in primary infections. We also assessed a possible contribution of basophils in immune responses to S. venezuelensis. By immunohistochemistry, we found that numbers of basophils and mast cells were markedly increased in the jejunal mucosa during primary infections with S. venezuelensis. Studies in basophil-deficient Mcpt8 DTR mice revealed a small but significant contribution of basophils to S. venezuelensis egg clearance in primary infections. Studies in mice deficient in various components of immune responses showed that CD4 ϩ T cells and ILC2 cells, IgG, FcR␥, and, to a lesser extent, IgE and FcRI contribute to effective immunity in primary S. venezuelensis infections. These findings support the conclusion that the hierarchy of importance of immune effector mechanisms in primary S. venezuelensis infection is as follows: CD4 ϩ T cells/ILC2 cells, IgG, and FcR␥Ͼ mast cellsϾIgE and FcRIϾbasophils. In contrast, in secondary S. venezuelensis infection, our evidence indicates that the presence of CD4 ϩ T cells is of critical importance but mast cells, antibodies, and basophils have few or no nonredundant roles.

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Section: Resultsmentioning

confidence: 84%

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

et al. 2017

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“…However, termination of infection clearly depends on a concerted action of innate effectors and the adaptive immune system, as infection was drastically prolonged for up to 1 year in T cell deficient nude mice (Dawkins et al 1982 a ). CD4 + T cells were the dominant cells contributing to timely termination of infection, since MHC-I −/− mice which lack CD8 + T cells displayed an unchanged course of S. venezuelensis infection whereas MHC-II −/− mice, which lack CD4 + T cells, displayed a delay in clearance of infection by 1 week (Goncalves et al 2008; Rodrigues et al 2009, 2013). As the authors did not quantify tissue migrating larvae, the net effect of absent CD4 + T cells could reflect specifically a less efficient eradication of migrating L3 as shown before in CD4 + T cell depleted mice for S. stercoralis (Rotman et al 1997) or a combination of less efficient eradication of tissue migrating L3 and expulsion of parasites from the intestine.…”

Section: Control and Eradication Of Parasitic Adults From The Intestimentioning

confidence: 99%

Strongyloides infection in rodents: immune response and immune regulation

Breloer

Abraham

2016

Parasitology

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The human pathogenic nematode Strongyloides stercoralis infects approximately 30-100 million people worldwide. Analysis of the adaptive immune response to S. stercoralis beyond descriptive studies is challenging, as no murine model for the complete infection cycle is available. However, the combined employment of different models each capable of modelling some features of S. stercoralis life cycle and pathology has advanced our understanding of the immunological mechanisms involved in host defence. Here we review: (i) studies using S. stercoralis third stage larvae implanted in diffusion chambers in the subcutaneous tissue of mice that allow analysis of the immune response to the human pathogenic Strongyloides species; (ii) studies using Strongyloides ratti and Strongyloides venezuelensis that infect mice and rats to extend the analysis to the parasites intestinal life stage and (iii) studies using S. stercoralis infected gerbils to analyse the hyperinfection syndrome, a severe complication of human strongyloidiasis that is not induced by rodent specific Strongyloides spp. We provide an overview of the information accumulated so far showing that Strongyloides spp. elicits a classical Th2 response that culminates in different, site specific, effector functions leading to either entrapment and killing of larvae in the tissues or expulsion of parasitic adults from the intestine.

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“…Previous studies from our group demonstrated that intestinal establishment of S. venezuelensis is affected by the absence of major histocompatibility complex (MHC) class II molecules during parasite infection. The MHC class II deficient mice (MHC II À/À ) presented higher susceptibility to S. venezuelensis infection, with impaired responses to the worm, suggesting that the failure of MHC class II expression affects the antigen presentation to CD4 + T cells that is necessary for the initiation of an effective Th2 response against the parasite (Abe and Nawa, 1988;Goncalves et al, 2008;Rodrigues et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Increased susceptibility to Strongyloides venezuelensis infection is related to the parasite load and absence of major histocompatibility complex (MHC) class II molecules

Rodrigues

Cardoso

Gonçalves

et al. 2013

Experimental Parasitology

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In human and murine models strongyloidiasis induce a Th2 type response. In the current study we investigated the role of different loads of Strongyloides venezuelensis in the immune response raised against the parasite and the participation of the major histocompatibility complex (MHC) class II molecule in the disease outcome in face of the different parasite burden. The C57BL/6 wild type (WT) and MHC II(-/-) mice were individually inoculated by subcutaneous injection with 500 or 3000 S. venezuelensis L3. The MHC II(-/-) mice infected with 3000L3 were more susceptible to S. venezuelensis infection when compared with WT groups, in which the parasite was completely eliminated. The production of Th2 cytokines and specific IgG1 or IgE antibodies against parasite were significantly lowered in MHC II(-/-) infected mice with different larvae inoculums. The infection of MHC II(-/-) mice with S. venezuelensis induced slight inflammatory alterations in the small intestine, and these lesions were lower when compared with WT mice, irrespective of the parasite load utilized to infect animals. Finally, we concluded that MHC class II molecules are essential in the immune response against S. venezuelensis mainly when infection occurs with high parasite inoculum.

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Immunolocalization and pathological alterations following Strongyloides venezuelensis infection in the lungs and the intestine of MHC class I or II deficient mice

Cited by 12 publications

References 31 publications

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

Strongyloides infection in rodents: immune response and immune regulation

Increased susceptibility to Strongyloides venezuelensis infection is related to the parasite load and absence of major histocompatibility complex (MHC) class II molecules

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Immunolocalization and pathological alterations following Strongyloides venezuelensis infection in the lungs and the intestine of MHC class I or II deficient mice

Cited by 12 publications

References 31 publications

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4+T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4+T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

Strongyloides infection in rodents: immune response and immune regulation

Increased susceptibility to Strongyloides venezuelensis infection is related to the parasite load and absence of major histocompatibility complex (MHC) class II molecules

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Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4⁺T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis