Type 2 Diabetes Mellitus and Increased Risk for Malaria Infection

Danquah, Ina; Bedu-Addo, George; Mockenhaupt, Frank P.

doi:10.3201/eid1610.100399

Cited by 91 publications

(95 citation statements)

References 13 publications

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“…Previous studies have shown that carriage of the sickle cell trait confers increased susceptibility to P. ovale infection ( 20 ) and that diabetes and HIV infection confer increased susceptibility to P. falciparum infection ( 30 ). …”

Section: Discussionmentioning

confidence: 99%

Comparison of ImportedPlasmodium ovale curtisiandP. ovale wallikeriInfections among Patients in Spain, 2005–2011

Marcos¹,

Rubio²,

Ramírez‐Olivencia³

et al. 2014

Emerg. Infect. Dis.

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Sequencing data from Plasmodium ovale genotypes co-circulating in multiple countries support the hypothesis that P. ovale curtisi and P. ovale wallikeri are 2 separate species. We conducted a multicenter, retrospective, comparative study in Spain of 21 patients who had imported P. ovale curtisi infections and 14 who had imported P. ovale wallikeri infections confirmed by PCR and gene sequencing during June 2005–December 2011. The only significant finding was more severe thrombocytopenia among patients with P. ovale wallikeri infection than among those with P. ovale curtisi infection (p = 0.031). However, we also found nonsignificant trends showing that patients with P. ovale wallikeri infection had shorter time from arrival in Spain to onset of symptoms, lower level of albumin, higher median maximum core temperature, and more markers of hemolysis than did those with P. ovale curtisi infection. Larger, prospective studies are needed to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

Comparison of ImportedPlasmodium ovale curtisiandP. ovale wallikeriInfections among Patients in Spain, 2005–2011

Marcos¹,

Rubio²,

Ramírez‐Olivencia³

et al. 2014

Emerg. Infect. Dis.

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“…Based on our current results, we speculate that this mechanism may contribute to the bacterial and viral infection susceptibility seen in patients with type 2 diabetes. Clinical reports have demonstrated that type 2 diabetic patients have a high risk for infection (26)(27)(28). Recent reports have shown that type 2 insulin resistance is tightly linked with S6K1 activity via a negative feedback loop involving S6K1 that suppresses insulin signaling under conditions of nutrient overload (29).…”

Section: Discussionmentioning

confidence: 99%

S6K1 Negatively Regulates TAK1 Activity in the Toll-Like Receptor Signaling Pathway

Kim

Baik

Baek

et al. 2014

Molecular and Cellular Biology

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dTransforming growth factor ␤ (TGF-␤)-activated kinase 1 (TAK1) is a key regulator in the signals transduced by proinflammatory cytokines and Toll-like receptors (TLRs). The regulatory mechanism of TAK1 in response to various tissue types and stimuli remains incompletely understood. Here, we show that ribosomal S6 kinase 1 (S6K1) negatively regulates TLR-mediated signals by inhibiting TAK1 activity. S6K1 overexpression causes a marked reduction in NF-B and AP-1 activity induced by stimulation of TLR2 or TLR4. In contrast, S6K1؊/؊ and S6K1 knockdown cells display enhanced production of inflammatory cytokines. Moreover, S6K1؊/؊ mice exhibit decreased survival in response to challenge with lipopolysaccharide (LPS). We found that S6K1 inhibits TAK1 kinase activity by interfering with the interaction between TAK1 and TAB1, which is a key regulator protein for TAK1 catalytic function. Upon stimulation with TLR ligands, S6K1 deficiency causes a marked increase in TAK1 kinase activity that in turn induces a substantial enhancement of NF-B-dependent gene expression, indicating that S6K1 is negatively involved in the TLR signaling pathway by the inhibition of TAK1 activity. Our findings contribute to understanding the molecular pathogenesis of the impaired immune responses seen in type 2 diabetes, where S6K1 plays a key role both in driving insulin resistance and modulating TLR signaling.T ransforming growth factor ␤-activated kinase 1 (TAK1) is a member of the mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) family (1). TAK1 is essential for the production of tumor necrosis factor (TNF-␣) and other inflammatory mediators by activating several MAPKs, such as p38␣ MAPK, Jun N-terminal protein kinases 1 and 2 (JNK1 and JNK2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2). TAK1 also plays a key regulatory role in several cytokine-mediated innate immunity signal transduction cascades, including interleukin-1 (IL-1) and the downstream signaling of Toll-like receptors (TLRs) and NOD1/2 (2, 3). In these pathways, various proinflammatory cytokines and TLR agonists trigger TAK1 activity, leading to its autophosphorylation and subsequent recruitment to the IB kinase (IKK) complex, ultimately resulting in the activation of the transcription factor NF-B and the upregulation of genes encoding proinflammatory cytokines, chemokines, adhesion molecules, and proteolytic enzymes.Several binding partners of TAK1, including TAK1-binding protein 1 (TAB1), TAB2, and TAB3, have been implicated in the regulation of TAK1 activity in response to various stimuli (1, 4). Previous reports demonstrated that the native forms of TAK1 comprise a catalytic kinase subunit in complex with the regulatory subunit TAB1 and either of two homologous proteins, TAB2 and TAB3 (2, 5, 6). Importantly, it has been reported that TAB1 might play a key role in the regulation of the TAK1 complex (7,8). Studies with TAB1-deficient mouse embryonic fibroblasts (TAB1 Ϫ/Ϫ MEFs) demonstrated that TAB1 is able to recruit p38␣ MAPK to the TAK1 complex f...

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“…Infection with malaria parasites can induce a rise in blood insulin levels above that of a normal healthy adult by as much as 10- to 35-fold [1, 2]. Given that the occurrence of type 2 diabetes is rising in malaria-endemic countries [3], compounded hyperinsulinemia in individuals affected by both diseases could become prevalent. In particular, a hallmark of type 2 diabetes is insulin resistance, which can often result in increased insulin secretion to compensate for the inability of the body to respond to insulin.…”

Section: Insulin and Insulin-like Growth Factor-1mentioning

confidence: 99%

The effects of ingested mammalian blood factors on vector arthropod immunity and physiology

Pakpour

Akman-Anderson

Vodovotz

et al. 2013

Microbes and Infection

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Type 2 Diabetes Mellitus and Increased Risk for Malaria Infection

Abstract: A case–control study of 1,466 urban adults in Ghana found that patients with type 2 diabetes mellitus had a 46% increased risk for infection with Plasmodium falciparum. Increase in diabetes mellitus prevalence may put more persons at risk for malaria infection.

Cited by 91 publications

References 13 publications

Comparison of ImportedPlasmodium ovale curtisiandP. ovale wallikeriInfections among Patients in Spain, 2005–2011

Comparison of ImportedPlasmodium ovale curtisiandP. ovale wallikeriInfections among Patients in Spain, 2005–2011

S6K1 Negatively Regulates TAK1 Activity in the Toll-Like Receptor Signaling Pathway

The effects of ingested mammalian blood factors on vector arthropod immunity and physiology

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