Concurrent gastro-intestinal nematode infection does not alter the development of experimental cerebral malaria

Souza, Brian de; Helmby, Helena

doi:10.1016/j.micinf.2008.04.015

Cited by 20 publications

(12 citation statements)

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“…In some animal models, helminth/malaria co-infected animals have been protected against severe malaria (18), whereas other studies report an increased susceptibility to severe disease (17) or no effect on severe disease whatsoever (56). More recently, Heligmosomoides polygyrus -infected mice immunized with blood-stage parasites of P. chabaudi chabaudi AS produced lower levels of malaria-specific Ab and of malaria-specific IFN-γ but higher levels of IL-4, IL-13, IL-10, and TGFβ (57), while others, using a similar model, showed that concurrent H. polygyrus had no effect on the development of cerebral malaria (56). …”

Section: Discussionmentioning

confidence: 99%

Patent Filarial Infection Modulates Malaria-Specific Type 1 Cytokine Responses in an IL-10-Dependent Manner in a Filaria/Malaria-Coinfected Population

Metenou

Dembele

Konaté

et al. 2009

The Journal of Immunology

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The effect of filarial infections on malaria-specific immune responses was investigated in Malian villages coendemic for filariasis (Fil) and malaria. Cytokines were measured from plasma and Ag-stimulated whole blood from individuals with Wuchereria bancrofti and/or Mansonella perstans infections (Fil+; n = 19) and those without evidence of filarial infection (Fil−; n = 19). Plasma levels of IL-10 (geometric mean [GM], 22.8 vs 10.4) were higher in Fil+ compared with Fil−, whereas levels of IFN-inducible protein (IP)-10 were lower in Fil+ (GM, 66.3 vs 110.0). Fil+ had higher levels of spontaneously secreted IL-10 (GM, 59.3 vs 6.8 pg/ml) and lower levels of IL-2 (1.0 vs 1.2 pg/ml) than did Fil−. Although there were no differences in levels of Staphylococcus aureus enterotoxin B-induced cytokines between the two groups, Fil+ mounted lower IL-12p70 (GM, 1.11 vs 3.83 pg/ml; p = 0.007), IFN-γ (GM, 5.44 vs 23.41 pg/ml; p = 0.009), and IP-10 (GM, 29.43 vs 281.7 pg/ml; p = 0.007) responses following malaria Ag (MalAg) stimulation compared with Fil−. In contrast, Fil+ individuals had a higher MalAg-specific IL-10 response (GM, 7318 pg/ml vs 3029 pg/ml; p = 0.006) compared with those without filarial infection. Neutralizing Ab to IL-10 (but not to TGFβ) reversed the down-regulated MalAg-specific IFN-γ and IP-10 (p < 0.001) responses in Fil+. Together, these data demonstrate that filarial infections modulate the Plasmodium falciparum-specific IL-12p70/IFN-γ secretion pathways known to play a key role in resistance to malaria and that they do so in an IL-10-dependent manner.

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Section: Discussionmentioning

confidence: 99%

Patent Filarial Infection Modulates Malaria-Specific Type 1 Cytokine Responses in an IL-10-Dependent Manner in a Filaria/Malaria-Coinfected Population

Metenou

Dembele

Konaté

et al. 2009

The Journal of Immunology

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“…Coinfection with Hp-Pb ANKA 2 weeks after initial helminthic infection did not modify the development of ECM despite accelerated Pb growth in vivo [149]. Likewise, other results from the same model of coinfection in BALB/c and C57BL/6 mice showed no differences in parasitemia, anemia, or body weight in relation to mice infected only with Plasmodium [150]. Therefore, Hp infection does not affect the outcome of Pb ANKA (Table 4(b)).…”

Section: Experimental Models Of Coinfectionmentioning

confidence: 99%

Helminth Parasites Alter Protection againstPlasmodiumInfection

Salazar-Castañón

Legorreta-Herrera

Rodrı́guez-Sosa

2014

BioMed Research International

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More than one-third of the world's population is infected with one or more helminthic parasites. Helminth infections are prevalent throughout tropical and subtropical regions where malaria pathogens are transmitted. Malaria is the most widespread and deadliest parasitic disease. The severity of the disease is strongly related to parasite density and the host's immune responses. Furthermore, coinfections between both parasites occur frequently. However, little is known regarding how concomitant infection with helminths and Plasmodium affects the host's immune response. Helminthic infections are frequently massive, chronic, and strong inductors of a Th2-type response. This implies that infection by such parasites could alter the host's susceptibility to subsequent infections by Plasmodium. There are a number of reports on the interactions between helminths and Plasmodium; in some, the burden of Plasmodium parasites increased, but others reported a reduction in the parasite. This review focuses on explaining many of these discrepancies regarding helminth-Plasmodium coinfections in terms of the effects that helminths have on the immune system. In particular, it focuses on helminth-induced immunosuppression and the effects of cytokines controlling polarization toward the Th1 or Th2 arms of the immune response.

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“…Therefore, when the other studies have found that adults with worms are still protected, we contend that this corresponds mostly to adults with comparatively lower worm loads who have achieved clinical immunity anyway. In support of this view, most studies of experimental co-infections in models, in which the worm load is usually high since it is an induced infection, concluded to their deleterious influence upon malaria [19], [20], [21], [22], with a single exception in a rodent model of cerebral malaria [23].…”

Section: Introductionmentioning

confidence: 98%

Understanding Human-Plasmodium falciparum Immune Interactions Uncovers the Immunological Role of Worms

Roussilhon

Brasseur

Agnamey³

et al. 2010

PLoS ONE

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BackgroundFormer studies have pointed to a monocyte-dependant effect of antibodies in protection against malaria and thereby to cytophilic antibodies IgG1 and IgG3, which trigger monocyte receptors. Field investigations have further documented that a switch from non-cytophilic to cytophilic classes of antimalarial antibodies was associated with protection. The hypothesis that the non-cytophilic isotype imbalance could be related to concomittant helminthic infections was supported by several interventions and case-control studies.Methods and FindingsWe investigated here the hypothesis that the delayed acquisition of immunity to malaria could be related to a worm-induced Th2 drive on antimalarial immune responses. IgG1 to IgG4 responses against 6 different parasite-derived antigens were analyzed in sera from 203 Senegalese children, half carrying intestinal worms, presenting 421 clinical malaria attacks over 51 months. Results show a significant correlation between the occurrence of malaria attacks, worm carriage (particularly that of hookworms) and a decrease in cytophilic IgG1 and IgG3 responses and an increase in non-cytophilic IgG4 response to the merozoite stage protein 3 (MSP3) vaccine candidate.ConclusionThe results confirm the association with protection of anti-MSP3 cytophilic responses, confirm in one additional setting that worms increase malaria morbidity and show a Th2 worm-driven pattern of anti-malarial immune responses. They document why large anthelminthic mass treatments may be worth being assessed as malaria control policies.

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Concurrent gastro-intestinal nematode infection does not alter the development of experimental cerebral malaria

Cited by 20 publications

References 20 publications

Patent Filarial Infection Modulates Malaria-Specific Type 1 Cytokine Responses in an IL-10-Dependent Manner in a Filaria/Malaria-Coinfected Population

Patent Filarial Infection Modulates Malaria-Specific Type 1 Cytokine Responses in an IL-10-Dependent Manner in a Filaria/Malaria-Coinfected Population

Helminth Parasites Alter Protection againstPlasmodiumInfection

Understanding Human-Plasmodium falciparum Immune Interactions Uncovers the Immunological Role of Worms

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