Gene polymorphisms in angiotensin I converting enzyme (ACE I/D) and angiotensin II converting enzyme (ACE2 C→T) protect against cerebral malaria in Indian adults

Dhangadamajhi, Gunanidhi; Mohapatra, Biswajit; Kar, Shantanu Kumar; Ranjit, Manoranjan

doi:10.1016/j.meegid.2010.01.009

Cited by 48 publications

(62 citation statements)

References 25 publications

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“…In this regard it is of interest that angiotensin-II has recently been shown to reduce erythrocyte invasion in vitro by P. falciparum in a dosedependent manner, and that the deletion allele of the ACE insertion/deletion polymorphism, which is associated with higher plasma ACE activity, has been reported to be protective against cerebral malaria (Dhangadamajhi et al, 2010;Saraiva et al, 2011). Further research into the question of whether the major genetic effects on plasma ACE activity at the ACE and ABO loci contribute significantly to differential susceptibility to severe malaria would be of interest.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Variation in Plasma Angiotensin‐I Converting Enzyme Activity Shows Allelic Heterogeneity in the ABO Blood Group Locus

Terao

Bayoumi

McKenzie

et al. 2013

Annals of Human Genetics

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SummaryAngiotensin-I converting enzyme (ACE) occupies a pivotal role in cardiovascular homeostasis. Major loci for plasma ACE have been identified at ACE on Chromosome 17 and at ABO on Chromosome 9. We sought to characterise the genetic architecture of plasma ACE at finer resolution in two populations. We carried out a GWAS in 1810 individuals of Japanese ethnicity; this identified signals at ACE and ABO that together accounted for nearly half of the population variability of the trait. We conducted measured haplotype analysis at the ABO locus in 1425 members of 248 British families using haplotypes of three SNPs, which together tagged the alleles responsible for the principal blood group antigens A1, A2, B and O. Type O alleles were associated with intermediate plasma ACE activity compared to Type A1 alleles (in whom plasma ACE activity was ∼36% lower) and Type B alleles (in whom plasma ACE activity was ∼36% higher). We demonstrated heterogeneity among A alleles: A2 alleles were associated with plasma ACE activity that was very similar to the O alleles. Variation at ACE accounted for 35% of the trait variance, and variation at ABO accounted for 15%. A further 10% could be ascribed to polygenic effects.

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Section: Discussionmentioning

confidence: 99%

Quantitative Variation in Plasma Angiotensin‐I Converting Enzyme Activity Shows Allelic Heterogeneity in the ABO Blood Group Locus

Terao

Bayoumi

McKenzie

et al. 2013

Annals of Human Genetics

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“…Several polymorphisms have been associated with higher prevalence of arterial hypertension; there are 2 polymorphisms in the Angiotensin Converting Enzyme (ACE) and Angiotensin Converting Enzyme 2 (ACE2) that lead to elevate circulating Ang II levels (Giner et al, 2000; Di Pasquale et al, 2004; Fan et al, 2007). Interestingly, these same genetic variations (the “D” allele of ACE I/D polymorphism and the ACE2 C→T substitution) have been associated with a lower incidence of cerebral malaria (CM) in Indian adults, although the later one only in women (Dhangadamajhi et al, 2010). …”

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confidence: 99%

“…Also, activation of AT2 receptor results in increased production of nitric oxide by endothelial Nitric Oxide Synthase (eNOS) in endothelial cells (Yayama and Okamoto, 2008), which could be protective against cerebral malaria since low nitric oxide bioavailability may exacerbate endothelial dysfunction and contributes to the pathogenesis of severe malaria (Gramaglia et al, 2006; Miller et al, 2013). Interestingly, polymorphisms in eNOS that are responsible for increased expression and nitric oxide production have been associated with mild malaria (Dhangadamajhi et al, 2009, 2010). …”

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confidence: 99%

Malaria and hypertension. Another co-evolutionary adaptation?

Gállego-Delgado

Rodrı́guez

2014

Front. Cell. Infect. Microbiol.

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“…Since substantial iRBC sequestration occurs in the microvasculature, this may be a strategy by which the parasite prevents vasoconstriction. Also angiotensin II (AT-II) promotes vasoconstriction, however, genetic polymorphisms in angiotensin I converting enzyme (ACE-I) or ACE-II, which result in increased levels of AT-II, are associated with protection against CM (Dhangadamajhi et al 2010). The latter finding may be related to the anti-plasmodial activity of AT-II (Torres et al 2015).…”

Section: Altered Vasomotor Activitymentioning

confidence: 99%

The immunological balance between host and parasite in malaria

Deroost

Pham

Opdenakker

et al. 2015

FEMS Microbiology Reviews

116

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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Gene polymorphisms in angiotensin I converting enzyme (ACE I/D) and angiotensin II converting enzyme (ACE2 C→T) protect against cerebral malaria in Indian adults

Cited by 48 publications

References 25 publications

Quantitative Variation in Plasma Angiotensin‐I Converting Enzyme Activity Shows Allelic Heterogeneity in the ABO Blood Group Locus

Quantitative Variation in Plasma Angiotensin‐I Converting Enzyme Activity Shows Allelic Heterogeneity in the ABO Blood Group Locus

Malaria and hypertension. Another co-evolutionary adaptation?

The immunological balance between host and parasite in malaria

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