Elevated Levels of Soluble TNF Receptors 1 and 2 Correlate with <i>Plasmodium falciparum</i> Parasitemia in Pregnant Women: Potential Markers for Malaria-Associated Inflammation

Thévenon, A; Zhou, Jun; Megnekou, Rosette; Ako, Simon Eyongabane; Leke, Rose G. F.; Taylor, Diane Wallace

doi:10.4049/jimmunol.1002293

Cited by 36 publications

(37 citation statements)

References 47 publications

(44 reference statements)

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“…In infected pregnant women, it has been shown that the soluble levels of TNF receptors are correlated with P. falciparum parasitemia (45). Moreover, systemic production of TNF-␣ has been observed following malaria infection during pregnancy and has been found to be associated with maternal anemia and low birth weight.…”

Section: Discussionmentioning

confidence: 97%

MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria

et al. 2014

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e Malaria is a widespread infectious disease caused by the parasite Plasmodium. During pregnancy, malaria infection leads to a range of complications that can affect both the mother and fetus, including stillbirth, infant mortality, and low birth weight. In this study, we utilized a mouse model of placental malaria (PM) infection to determine the importance of the protein MyD88 in the host immune response to Plasmodium during pregnancy. Initially, we demonstrated that Plasmodium berghei NK65GFP adhered to placental tissue via chondroitin sulfate A and induced PM in mice with a C57BL/6 genetic background. To evaluate the involvement of MyD88 in the pathology of PM, we performed a histopathological analysis of placentas obtained from MyD88 ؊/؊ and wild-type (WT) mice following infection on the 19th gestational day. Our data demonstrated that the detrimental placental alterations observed in the infected mice were correlated with the expression of MyD88. Moreover, in the absence of this protein, production of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-␣) was significantly reduced in the infected mice. More importantly, in contrast to fetuses from infected WT mice, which exhibited a reduction in body weight, the fetuses from infected MyD88 ؊/؊ mice did not display significant weight loss compared to their noninfected littermates. In addition, we observed a decrement of maternal care associated with malaria infection, which was attenuated in the MyD88-deficient mice. Collectively, the results of this study illustrate the pivotal importance of the MyD88 signaling pathway in the pathogenesis of placental malaria, thus presenting new possibilities for targeting MyD88 in therapeutic interventions.

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Section: Discussionmentioning

confidence: 97%

MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria

et al. 2014

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“…In asymptomatically infected pregnant women, parasite density is correlated to the levels of soluble mediators of inflammation, such as soluble TNF receptors (TNF-R1 and TNF-R2), IL-10 and G-CSF, suggesting these factors may represent markers of PAM-related inflammation [28, 29]. Altered DCs and monocytes, and reduced frequency and low expression of the CD86 and CD80 activation markers, are observed in malaria-infected pregnant women, suggesting DC migration to lymphoid organs [30].…”

Section: Introductionmentioning

confidence: 99%

Usefulness of a biomarker to identify placental dysfunction in the context of malaria

Gueneuc

Deloron

Bertin

2017

Malar J

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In most tropical areas, pregnant women are at increased risk of malaria, as a consequence of the massive sequestration of parasitized red blood cells in the placenta. The placenta plays a key role in embryonic and fetal development as well as in maternal-fetal exchanges, and pregnancy-associated malaria may alter selected placenta functions that lead to stillbirth and low birth weight. Although there are several tools (blood smear examination, RDT, PCR) to diagnose malaria infection during pregnancy, there is currently no test to assess placenta dysfunction in the framework of pregnancy-associated malaria. Pregnancy-associated malaria shares many features with preeclampsia, an extensively studied disease. Various biomarkers associated with placental dysfunction have been identified as associated with preeclampsia. Several of these are inflammatory markers that lack of specificity. A few seem more specific of placenta dysfunction, including s-endoglin and sFlt1, increased in the peripheral blood during preeclampsia. The predictive value of these biomarkers should be studied in the context of pregnancy-associated malaria to evaluate their usefulness in identifying placental dysfunction during malaria. These biomarkers should be considered to improve the diagnosis of placental dysfunction during malaria and pregnant women monitoring.

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“…19,20 However, the origin of sTNFR2 in serum remains unclear. In the present study, we show for the first time that sTNFR2 in serum originates not only from BM-derived cells but also from non-BM-derived cells in LPS-induced septic shock.…”

Section: Discussionmentioning

confidence: 99%

“…The origin and function of this molecule are still not clear, although its presence correlates with an unfavorable prognosis in some cases. 19,20,36 To answer this question, dynamic changes in levels of sTNFR2 in serum in the different groups of mice described above were studied at 0, 1.5, 6 and 48 h after LPS injection. Without LPS stimulation, serum sTNFR2 concentrations in WT.WT chimera were similar to those of age-matched control WT mice (data not shown), indicating that irradiation and BM reconstitution did not significantly affect sTNFR2 release.…”

Section: Non-bm Tnfr2 Contributes To Lps Sensitivity Sb Liu Et Al 166mentioning

confidence: 99%

“…18 Similar to TNF, elevated levels of soluble TNFR2 (sTNFR2) in serum or other body fluids has been recognized as a predictor of pathological conditions, such as sepsis, infections, hepatitis, organ fibrosis, cancer development and other inflammatory diseases. 19,20 In vitro experiments demonstrated that sTNFR2 can be rapidly shed from activated BM-derived cells, such as neutrophils and cultured mononuclear cells, upon TNF, lipopolysaccharide (LPS) or IL-10 stimulation. 21,22 The origin of non-BM-derived sTNFR2 in serum has not yet been formally demonstrated, especially during inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

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TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum

et al. 2011

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Persistently high serum levels of soluble tumor-necrosis factor (TNF) receptor 2 (sTNFR2) have been observed in septic shock and many inflammatory diseases. However, its origin and regulation during these pathological processes are still largely unknown. In this study, murine bone marrow (BM) chimeras selectively expressing TNFR2 on either BM-derived or non-BM-derived cells were generated and challenged with lipopolysaccharide (LPS). The results show that TNFR2 expression on non-BM-derived cells is crucial for both the sensitivity of mice to LPS and the downregulation of sTNFR2 in serum. Most importantly, sTNFR2 was released from both BM-and non-BM-derived cells. Non-BM TNFR1 expression influenced the sensitivity of mice to LPS challenge but not the level of serum sTNFR2. These results provide the first in vivo evidence for the origin and regulation of sTNFR2 in serum and could aid in the development of novel anti-TNF strategies against septic shock.

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Elevated Levels of Soluble TNF Receptors 1 and 2 Correlate with Plasmodium falciparum Parasitemia in Pregnant Women: Potential Markers for Malaria-Associated Inflammation

Cited by 36 publications

References 47 publications

MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria

MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria

Usefulness of a biomarker to identify placental dysfunction in the context of malaria

TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum

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