Maturation of the filaria<i>Litomosoides sigmodontis</i>in BALB/c mice; comparative susceptibility of nine other inbred strains

Petit, G.; Diagne, Moussa Moïse; Maréchal, Pierre Le; Owen, David J.; Taylor, D. J.; Bain, O.

doi:10.1051/parasite/1992675144

Cited by 114 publications

(144 citation statements)

References 5 publications

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“…7 microfilariae/10 mm 3 (Petit et al 1992). BALB/c mice were purchased from Charles River, IFFA, CREDO and Harlan, France.…”

Section: Rodents and Infestationsmentioning

confidence: 99%

“…The rodent was therefore placed on ice, in order to immobilize the filarial worms and block suction mechanisms. We studied haematophagy in 2 hosts, the Mongolian gerbil Meriones unguiculatus, where microfilaraemia reaches high levels, and the BALB/c mouse, a strain susceptible to L. sigmodontis (Petit et al 1992) although with lower microfilaraemia than the gerbil. A high number of filarial worms of both sexes was examined at different stages of development from young 4th-stage larvae at day 9 post-infection to late adult stages at day 330 p.i.…”

Section: Introductionmentioning

confidence: 99%

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Blood-feeding in the young adult filarial wormsLitomosoides sigmodontis

Attout

Babayan

Hoerauf³

et al. 2004

Parasitology

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In this study with the filarial model Litomosoides sigmodontis, we demonstrate that the worms ingest host red blood cells at a precise moment of their life-cycle, immediately after the fourth moult. The red blood cells (RBC) were identified microscopically in live worms immobilized in PBS at 4 xC, and their density assessed. Two hosts were used : Mongolian gerbils, where microfilaraemia is high, and susceptible BALB/c mice with lower microfilaraemia. Gerbils were studied at 12 time-points, between day 9 post-inoculation (the worms were young 4th stage larvae) and day 330 p.i. (worms were old adults). Only the very young adult filarial worms had red blood cells in their gut. Haematophagy was observed between days 25 and 56 p.i. and peaked between day 28 and day 30 p.i. in female worms. In males, haematophagy was less frequent and intense. Similar kinetics of haematophagy were found in BALB/c mice, but frequency and intensity tended to be lower. Haematophagy seems useful to optimize adult maturation. These observations suggest that haematophagy is an important step in the life-cycle of L. sigmodontis. This hitherto undescribed phenomenon might be characteristic of other filarial species including human parasites.

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“…7 microfilariae/10 mm 3 (Petit et al 1992). BALB/c mice were purchased from Charles River, IFFA, CREDO and Harlan, France.…”

Section: Rodents and Infestationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blood-feeding in the young adult filarial wormsLitomosoides sigmodontis

Attout

Babayan

Hoerauf³

et al. 2004

Parasitology

Self Cite

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“…The discovery that the filarial nematode L. sigmodontis will follow its full natural course of infection within certain mouse strains (35) now provides an immunological model to study these events in the context of full infection. Only with this model can one ask which immunoregulatory events allow the infective L3 stage to migrate from skin entry sites to the pleural cavity, to develop there into mature adult parasites, and to establish a patent infection with Mf circulating within the bloodstream.…”

mentioning

confidence: 99%

F4/80+ Alternatively Activated Macrophages Control CD4+ T Cell Hyporesponsiveness at Sites Peripheral to Filarial Infection

Taylor

Harris

Nair

et al. 2006

The Journal of Immunology

105

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Both T cells and APC have been strongly implicated in the immune suppression observed during filarial nematode infections, but their relative roles are poorly understood, particularly in regard to timing and locality of action. Using Litomosoides sigmodontis infection of susceptible BALB/c mice, we have studied the progression of filarial immunosuppression leading to patent infection with blood microfilaremia. Patent infection is associated with decreased immune responsiveness in the draining thoracic lymph nodes (tLN) and intrinsically hyporesponsive CD4+ T cells at the infection site. We now show that we are able to separate, both in time and space, different suppressive mechanisms and cell populations that contribute to filarial hyporesponsiveness. L. sigmodontis infection recruited a F4/80+ population of alternatively activated macrophages that potently inhibited Ag-specific CD4+ T cell proliferative responses even in the presence of competent naive APC. T cell responsiveness was partially restored by neutralizing TGF-β, but not by blocking IL-10 or CTLA-4 signaling. During prepatent infection, the macrophage population was restricted to the infection site. However, once infection became patent with systemic release of microfilariae, the suppressive macrophage activity extended peripherally into the tLN. In contrast, the hyporesponsive CD4+ T cell phenotype remained localized at the infection site, and the tLN CD4+ T cell population recovered full Ag responsiveness in the absence of suppressive macrophages. Filarial immunosuppression, therefore, evolves over time at sites increasingly distal to infection, and the mechanisms of filarial down-regulation are dependent on proximity to the infection site.

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“…L. sigmodontis third-stage larvae (L3) are transmitted to their natural host, the cotton rat (Sigmodon hispidus), by the bite of infected mites (Ornithonyssus bacoti). Laboratory mice may be infected naturally by the bite of infected mites (19,20) or artificially by injection of L3 (21) or implantation of different stages such as L3, adults, and first-stage larvae, socalled microfilariae (MF) (22). After infection, L3 migrate during the first 3 d via the lymphatic system to the thoracic cavity (23).…”

mentioning

confidence: 99%

Pathogenic Nematodes Suppress Humoral Responses to Third-Party Antigens In Vivo by IL-10–Mediated Interference with Th Cell Function

Hartmann

Haben

Fleischer

et al. 2011

The Journal of Immunology

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One third of the human population is infected with helminth parasites. To promote their longevity and to limit pathology, helminths have developed several strategies to suppress the immune response of their host. As this immune suppression also acts on unrelated third-party Ags, a preexisting helminth infection may interfere with vaccination efficacy. In this study, we show that natural infection with Litomosoides sigmodontis suppressed the humoral response to thymus-dependent but not to thymus-independent model Ags in C57BL/6 mice. Thereby, we provide evidence that reduced humoral responses were mediated by interference with Th cell function rather than by direct suppression of B cells in L. sigmodontis-infected mice. We directly demonstrate suppression of Ag-specific proliferation in OVA-specific Th cells after adoptive transfer into L. sigmodontis-infected mice that led to equally reduced production of OVA-specific IgG. Transferred Th cells displayed increased frequencies of Foxp3+ after in vivo stimulation within infected but not within naive mice. Helminth-mediated suppression was induced by established L. sigmodontis infections but was completely independent of the individual worm burden. Using DEREG mice, we rule out a central role for host-derived regulatory T cells in the suppression of transferred Th cell proliferation. In contrast, we show that L. sigmodontis-induced, host-derived IL-10 mediated Foxp3 induction in transferred Th cells and significantly contributed to the observed Th cell hypoproliferation within infected mice.

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Maturation of the filariaLitomosoides sigmodontisin BALB/c mice; comparative susceptibility of nine other inbred strains

Cited by 114 publications

References 5 publications

Blood-feeding in the young adult filarial wormsLitomosoides sigmodontis

Blood-feeding in the young adult filarial wormsLitomosoides sigmodontis

F4/80+ Alternatively Activated Macrophages Control CD4+ T Cell Hyporesponsiveness at Sites Peripheral to Filarial Infection

Pathogenic Nematodes Suppress Humoral Responses to Third-Party Antigens In Vivo by IL-10–Mediated Interference with Th Cell Function

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