Malaria: toxins, cytokines and disease

Jakobsen, Palle; Bate, Clive; Taverne, Janice; Playfair, John

doi:10.1111/j.1365-3024.1995.tb01019.x

Cited by 61 publications

(33 citation statements)

References 73 publications

(47 reference statements)

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“…Malaria infections are complicated syndromes involving many inflammatory host-derived factors such as cytokines. Parasite antigenic products stimulate the overproduction of tumour necrosis factor alpha (TNF-), interferon gamma (IFN-) and interleukin-1 (IL-1), which adversely affect disease progression [16]. These cytokines, among other effects, cause changes in the host such as fever, suppression of bone marrow and erythrocyte production, coupled with direct destruction of host erythrocytes [17].…”

Section: Discussionmentioning

confidence: 99%

Characterization and Treatment of Severe Malaria in Hospitalized Children at a Ghanaian District Hospital

Gyapong¹,

Duwiejua²,

Bio³

et al. 2009

TOTMJ

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Abstract:Objective: To document the demography of paediatric admissions due to severe malaria, presentation and determinants of clinical symptoms and treatment for the condition at the KNUST Hospital, Ghana.Methods: A prospective, non-randomized, observational study was undertaken at the Children's Ward of the KNUST Hospital, in Kumasi. During a one month period, the symptoms on admission, treatment and treatment outcome of included children were documented. Inclusion criteria were age 0-144 months, verbal informed consent and severe malaria defined by presence of asexual Plasmodium falciparum parasitaemia coupled with at least one criterion suggestive of severe malaria as defined by WHO.Results: Overall, there were 82 malaria admissions with 69 cases being enrolled. On admission, mean haemoglobin levels were consistent for both males and females. Mean body weight was higher for females. Main presentations were anaemia of moderate to severe form (56); fever (52) and convulsions (24). Prostration was observed in all cases. Children under 5 years of age were associated with anaemia (p=0.018) and neurological symptoms (p=0.003). Clinical presentation of severe malaria was found to be independent of patients' sex. Quinine was used as treatment in 17 cases; monotherapy with artemisinin derivatives in 26 cases and artemisinin-amodiaquine combinations in 19 of the cases. No deaths were recorded. Conclusions:Children under 5 years of age presented more often with severe malaria. Prostration, anaemia and neurological symptoms were the most frequent manifestations.

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Section: Discussionmentioning

confidence: 99%

Characterization and Treatment of Severe Malaria in Hospitalized Children at a Ghanaian District Hospital

Gyapong¹,

Duwiejua²,

Bio³

et al. 2009

TOTMJ

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“…Thus, sequestration of PRBC depends on the number or type of the cytoadhesion molecules induced in the course of infection by stimulation of upregulating factors, including cytokines such as TNF-␣ 4,8 Tumor necrosis factor-alpha release is considered to be caused by activation of cells such as monocytes by parasitederived ''toxins'' containing glycosylphosphatidyl inositol (GPI). 9,10 However, IgE complexes with antigen or with IgG anti-IgE may also induce TNF-␣ release from certain cell types equipped with Fc (fragment, crystalline) receptors for this immunoglobulin isotype. 11 The expression on monocytes of CD23, a low affinity Fc-receptor for IgE, correlates with IgE elevation occurring in the course of parasitic infections.…”

Section: Introductionmentioning

confidence: 99%

IgE deposition in brain microvessels and on parasitized erythrocytes from cerebral malaria patients.

Maeno¹,

Perlmann²,

PerlmannH³

et al. 2000

The American Journal of Tropical Medicine and Hygiene

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Abstract. Postmortem brain tissues of 21 cerebral malaria cases were obtained in Myanmar and Vietnam. The tissues were examined by light microscopy and by an immunohistochemical method. Brain microvessels (capillaries and venules) were examined for the presence of immunoglobulins IgE and IgG, Plasmodium falciparum antigen, and parasitized erythrocytes (PRBC). Deposition of IgE, IgG, and P. falciparum antigen was observed in the microvessels from all specimens examined. Sequestered PRBC in the microvessels were positive for IgG in all 21 cases and for IgE in six cases. In the latter cases, the percentage of microvessels with sequestered PRBC was Ͼ 50%, with the frequency of IgE-positive cells ranging from 42% to 52%. In contrast, in five cases that were only weakly positive for IgE, the percentage of microvessels with sequestered PRBC was remarkably low (Ͻ 1%). These data indicate that the degree of deposition of IgE in microvessels and on PRBC from cerebral malaria patients correlated with that of PRBC sequestration. As IgE-containing immune complexes are known to induce local overproduction of tumor necrosis factor-alpha (TNF-␣), a major pathogenic factor in cerebral malaria, IgE may contribute to the pathogenesis of this severe disease.

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“…Thus, clinical immunity to malaria may indeed be immunotolerance and absence of allergic-type responses rather than the presence of neutralising antibodies to malaria "toxins" as previously suggested (Jakobsen et al, 1995). Several lines of additional evidence support the concept that susceptibility to malaria and atopy may be related to the same immunological defect.…”

Section: Role Of Allergy In Malariamentioning

confidence: 52%