Association of TNF level with production of circulating cellular microparticles during clinical manifestation of human cerebral malaria

Sahu, Upasana; Sahoo, Prakash Kumar; Kar, Shantanu Kumar; Mohapatra, Biswajit; Ranjit, Manoranjan

doi:10.1016/j.humimm.2013.02.006

Cited by 48 publications

(55 citation statements)

References 39 publications

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“…Point (3) for the cytokine hypothesis is questionable with some studies showing a clear increase in TNF in CM, which is even higher in fatal cases in African children (Grau et al, 1989; Kwiatkowski et al, 1990; Sahu et al, 2013), but more recent studies have shown no correlation between TNF concentration and CM (Esamai et al, 2003; Armah et al, 2007; Thuma et al, 2011). Other cytokines have been implicated too (Hunt and Grau, 2003; Boeuf et al, 2012; Ioannidis et al, 2014), but the results of these studies are hard to interpret as it depends on which control group it is compared to; NCM, severe malarial anemia, other encephalitis, other febrile illnesses or even healthy individuals.…”

Section: Pathogenesis Of CMmentioning

confidence: 99%

“…Soluble ICAM-1 does seem to correlate with CM (Adukpo et al, 2013), but depending on the comparator control group (UM or other SM) it seems more strongly associated with SM (Cserti-Gazdewich et al, 2010; Erdman et al, 2011). Circulating endothelial microparticles are also associated with SM only in adults (Sahu et al, 2013) but do correlate with CM in children (Combes et al, 2004). …”

Section: Pathogenesis Of CMmentioning

confidence: 99%

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Pathogenesis of cerebral malariaâ€”inflammation and cytoadherence

Storm

Craig

2014

Front. Cell. Infect. Microbiol.

143

138

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Despite decades of research on cerebral malaria (CM) there is still a paucity of knowledge about what actual causes CM and why certain people develop it. Although sequestration of P. falciparum infected red blood cells has been linked to pathology, it is still not clear if this is directly or solely responsible for this clinical syndrome. Recent data have suggested that a combination of parasite variant types, mainly defined by the variant surface antigen, P. falciparum erythrocyte membrane protein 1 (PfEMP1), its receptors, coagulation and host endothelial cell activation (or inflammation) are equally important. This makes CM a multi-factorial disease and a challenge to unravel its causes to decrease its detrimental impact.

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Section: Pathogenesis Of CMmentioning

confidence: 99%

Section: Pathogenesis Of CMmentioning

confidence: 99%

Pathogenesis of cerebral malariaâ€”inflammation and cytoadherence

Storm

Craig

2014

Front. Cell. Infect. Microbiol.

143

138

View full text Add to dashboard Cite

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“…B. brevis was acquired in R2, with R1 as the TruCOUNT TM beads gate. The number of cells was calculated by the following formula (Sahu et al, 2013): Cell number (events in R2)…”

Section: Effect Of Pollutant On Cell Growthmentioning

confidence: 99%

Biosorption and biodegradation of pyrene by Brevibacillus brevis and cellular responses to pyrene treatment

Liao

Chen

Peng

et al. 2015

Ecotoxicology and Environmental Safety

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“…MPs derived from iRBCs are more potent in activating macrophages than iRBCs, an effect mediated by TLR4 and MyD88-signalling (Couper et al 2010). These circulating MPs are highly associated with CM in both humans and mice (Combes et al 2005;Pankoui Mfonkeu et al 2010;Sahu et al 2013). MPs produced by other cell types including ECs, leukocytes and platelets, are also implicated in malaria pathology but will be discussed later (see Section 'Inflammation').…”

Section: Mps and Exosomesmentioning

confidence: 99%

The immunological balance between host and parasite in malaria

Deroost

Pham

Opdenakker

et al. 2015

FEMS Microbiology Reviews

111

143

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One sentence summary: The intricate balance between anti-malarial immunity and parasite virulence factors including immune evasion mechanisms determine the outcome of malaria infections, as imbalances resulting in exaggerated parasite growth, excessive inflammation or the combination of both result in severe pathology. Editor: Christian van Ooij ABSTRACTCoevolution of humans and malaria parasites has generated an intricate balance between the immune system of the host and virulence factors of the parasite, equilibrating maximal parasite transmission with limited host damage. Focusing on the blood stage of the disease, we discuss how the balance between anti-parasite immunity versus immunomodulatory and evasion mechanisms of the parasite may result in parasite clearance or chronic infection without major symptoms, whereas imbalances characterized by excessive parasite growth, exaggerated immune reactions or a combination of both cause severe pathology and death, which is detrimental for both parasite and host. A thorough understanding of the immunological balance of malaria and its relation to other physiological balances in the body is of crucial importance for developing effective interventions to reduce malaria-related morbidity and to diminish fatal outcomes due to severe complications. Therefore, we discuss in this review the detailed mechanisms of anti-malarial immunity, parasite virulence factors including immune evasion mechanisms and pathogenesis. Furthermore, we propose a comprehensive classification of malaria complications according to the different types of imbalances.

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Association of TNF level with production of circulating cellular microparticles during clinical manifestation of human cerebral malaria

Cited by 48 publications

References 39 publications

Pathogenesis of cerebral malariaâ€”inflammation and cytoadherence

Pathogenesis of cerebral malariaâ€”inflammation and cytoadherence

Biosorption and biodegradation of pyrene by Brevibacillus brevis and cellular responses to pyrene treatment

The immunological balance between host and parasite in malaria

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