Chronic giardiasis in B-cell-deficient mice expressing the xid gene

Snider, Denis P.; Skea, Danna L.; Underdown, Brian J.

doi:10.1128/iai.56.11.2838-2842.1988

Cited by 34 publications

(17 citation statements)

References 19 publications

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“…X-linked immunodeficiency affects resistance to several infections. Thus, CBA/N mice are highly susceptible to infection with different strains of type 3 Streptococcus pneumoniae [39,40], Giardia muris [41], Plasmodium yoelli [42], Pseudomonas aeruginosa [43], and Salm. typhimurium [44].…”

Section: Discussionmentioning

confidence: 99%

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

Никоненко

Apt

Mezhlumova

et al. 1996

Clinical and Experimental Immunology

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SUMMARYWe have studied the role of three mouse distinct non-H-2 genes (Bcg, Tbc-1, xid ) in several phenomena of antituberculosis immunity and resistance. On the basis of median survival time (MST) of mice following infection with virulent Mycobacterium tuberculosis H37Rv, Bcg gene did not control resistance to the lethal dose of H37Rv infection in non-vaccinated and Myco. bovis (BCG)-vaccinated mice. However, Bcg r allele, in comparison with Bcg s allele, determined more effective suppression of an early multiplication in spleens of H37Rv mycobacteria after a low dose (5 2 10 4 colony-forming units (CFU)) injection. CBA/N mice, which are not protected efficiently against tuberculous challenge by BCG vaccination, were characterized by a decreased in vitro proliferation of immune lymph node cells, both spontaneous and stimulated with mycobacterial antigens. The decreased proliferation was due to immunosuppression caused by interactions between responding T cells and CBA/N antigen-presenting cells (APC). We have confirmed that the defective response to BCG-vaccination in CBA/N mice is linked with the X-chromosome and thus is presumably determined by the xid gene itself. I/St mice (Tbc-1 s ), supersusceptible to H37Rv infection, were not able to restrict the growth of H37Rv mycobacteria in spleens, even following infection with a low dose (5 2 10 4 ), but restricted the growth of Myco. bovis BCG more effectively than Bcg s mice.

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Section: Discussionmentioning

confidence: 99%

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

Никоненко

Apt

Mezhlumova

et al. 1996

Clinical and Experimental Immunology

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“…Such antibodies reach their targets in vivo , since anti‐giardial IgA antibodies coat trophozoites in Giardia ‐infected mice (30). Mice depleted of B cells by treatment with anti‐IgM antibodies and mice with X‐linked immunodeficiency, which have a defect in B cell development and function, are unable to clear G. muris infection (33,34). Furthermore, B cell‐deficient mice generated by gene targeting are unable to clear infections with G. muris or G. lamblia GS/M‐H7 (35,36).…”

Section: Mucosal Defence Mechanisms Against Giardiamentioning

confidence: 99%

Mucosal defences against Giardia

Eckmann

2003

Parasite Immunology

199

166

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Giardia lamblia (syn. G. duodenalis or G. intestinalis), the causative agent of giardiasis, is one of the most common causes worldwide of intestinal infections in humans. Symptomatic infection is characterized by diarrhoea, epigastric pain, nausea, vomiting, and weight loss, yet many infections are asymptomatic. The protozoan, unicellular parasite resides in the lumen and attaches to the epithelium and overlying mucus layers but does not invade the mucosa and causes little or no mucosal inflammation. Giardiasis is normally transient, indicating the existence of effective host defences, although re-infections can occur, which may be related to differences in infecting parasites and/or incomplete immune protection. Mucosal defences against Giardia must act in the small intestinal lumen in the absence of induction by classical inflammatory mediators. Secretory IgA antibodies have a central role in anti-giardial defence. B cell-independent mechanisms also exist and can contribute to eradication of the parasite, although their identity and physiological importance are poorly understood currently. Possible candidates are nitric oxide, antimicrobial peptides such as Paneth cell alpha-defensins, and lactoferrin. Elucidation of the key anti-giardial effector mechanisms will be important for selecting the best adjuvants in the rational development of vaccination strategies against Giardia.

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“…Giardia lamblia infections in humans induce immune response characterized by production of large amounts of anti‐parasite IgA (reviewed in (1,3)). IgA is required for prevention of chronic G. muris , a rodent specific species of Giardia, infections in mice (5–8). In contrast, in the adult mouse model of G. lamblia infection, antibodies are not required to eliminate the parasite and a cellular immune response is able to control the infection in the absence of antibodies (8–11).…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor α contributes to protection against Giardia lamblia infection in mice

Zhou

Shea‐Donohue

et al. 2007

Parasite Immunology

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Giardia lamblia is a ubiquitous parasite that causes diarrhoea. Effective control of Giardia infections in mice has been shown to involve IgA, T cells, mast cells and IL-6. We now show that Tumour necrosis factor alpha (TNFalpha) also plays an important role in the early control of giardiasis. Mice treated with neutralizing anti-TNFalpha antibodies or genetically deficient in TNFalpha were infected with the G. lamblia clone GS/(M)-H7. In both cases, mice lacking TNFalpha had much higher parasite numbers than controls during the first 2 weeks of infections. However, anti-parasite IgA levels, mast cell responses, and IL-4 and IL-6 mRNA levels do not appear significantly altered in the absence of TNFalpha. In addition, we show that mice infected with G. lamblia exhibit increased intestinal permeability, similar to human Giardia infection, and that this increase occurs in both wild-type and TNFalpha deficient mice. We conclude that TNFalpha is essential for host resistance to G. lamblia infection, and that it does not exert its effects through mechanisms previously implicated in control of this parasite.

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Chronic giardiasis in B-cell-deficient mice expressing the xid gene

Cited by 34 publications

References 19 publications

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

Mucosal defences against Giardia

Tumour necrosis factor α contributes to protection against Giardia lamblia infection in mice

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