scholarly journals Interferon-γ and Interleukin-10 Responses during Clinical Malaria Episodes in Infants Aged 0–2 Years Prenatally Exposed to Plasmodium falciparum: Tanzanian Birth Cohort

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Boniphace Sylvester ◽  
Dinah B. Gasarasi ◽  
Said Aboud ◽  
Donath Tarimo ◽  
Siriel Masawe ◽  
...  

Background. Infants born to mothers with placental malaria are prenatally exposed to Plasmodium falciparum antigens. However, the effect of that exposure to subsequent immune responses has not been fully elucidated. This study aimed at determining the effect of prenatal exposure to P. falciparum on Interleukin-10 and Interferon-γ responses during clinical malaria episodes in the first 24 months of life. Methods. This prospective cohort study involved 215 infants aged 0-2 years born to mothers with or without placental malaria. Enzyme-linked immunosorbent assay (ELISA) was used to determine levels of IL-10 and IFN-γ in infants and detect IgM in cord blood. Data were analyzed using SPSS version 20. Findings. Geometric mean for IFN-γ in exposed infants was 557.9 pg/ml (95% CI: 511.6-604.1) and in unexposed infants it was 634.4 pg/ml (95% CI: 618.2-668.5) (P=0.02). Mean IL-10 was 22.4 pg/ml (95% CI: 19.4-28.4) and 15.1 pg/ml (95%CI: 12.4-17.6), respectively (P=0.01). Conclusions. Prenatal exposure to P. falciparum antigens significantly affects IL-10 and IFN-γ responses during clinical malaria episodes in the first two years of life.

2021 ◽  
Vol 1 (2) ◽  
pp. 30-38
Author(s):  
Okezie C. Okamgba

Background: Placental malaria is a major cause of infection induced adverse conditions in pregnancy and is attributed to the sequestration of malaria parasite in the intervillous space. We investigated if any relationship exists between the parasite density and cytokines in malaria parasite infected human placentas. Methods: Sixty (60) malaria parasite infected placentas from apparently healthy immediate post-partum women and 40 malaria parasite uninfected placentas which served as control were studied. Blood from the human placenta was aseptically collected and tested for HIV and malaria parasite using standard methods. Interferon-Gamma (IFNγ), Tumor Necrosis Factor alpha (TNFα), Interleukin-4 (IL-4), Interleukin-6 (IL-6) and Interleukin-10 (IL-10) were measured by Enzyme-Linked Immunosorbent Assay (ELISA) technique. Data were analysed using appropriate statistical tools. Results: The result revealed P. falciparum with a mean parasite density of 762.47±459.62 parasite/μl of blood. The mean±SD (11.71±6.55pg/ml) and 55.57±43.13pg/ml for IFNγ and IL-10 respectively for infected placenta was statistically higher on comparison with 5.58±2.86pg/ml and 16.60±4.88pg/ml for IFNγ and IL10 respectively for uninfected human placenta (P<0.05). Positive correlation existed between parasite density and IL-6 (r = 0.59, p = 0.001) and between parasite density and IL-10 (r =0.41, p=0.024). Conclusion: The study showed upregulated levels of IL-6 and IL-10 which indicates disruption of normal immune balance in the parasite infected placenta and the amount of IL-6 and IL-10 secreted could reflect the level of parasitaemia and could serve for diagnostic assessment of placental malaria.


2021 ◽  
Vol 6 ◽  
pp. 79
Author(s):  
John W.G. Addy ◽  
Yaw Bediako ◽  
Francis M. Ndungu ◽  
John Joseph Valetta ◽  
Adam J. Reid ◽  
...  

Background: Studies of long-term malaria cohorts have provided essential insights into how Plasmodium falciparum interacts with humans, and influences the development of antimalarial immunity. Immunity to malaria is acquired gradually after multiple infections, some of which present with clinical symptoms. However, there is considerable variation in the number of clinical episodes experienced by children of the same age within the same cohort. Understanding this variation in clinical symptoms and how it relates to the development of naturally acquired immunity is crucial in identifying how and when some children stop experiencing further malaria episodes. Where variability in clinical episodes may result from different rates of acquisition of immunity, or from variable exposure to the parasite. Methods: Using data from a longitudinal cohort of children residing in an area of moderate P. falciparum transmission in Kilifi district, Kenya, we fitted cumulative episode curves as monotonic-increasing splines, to 56 children under surveillance for malaria from the age of 5 to 15. Results: There was large variability in the accumulation of numbers of clinical malaria episodes experienced by the children, despite being of similar age and living in the same general location. One group of children from a particular sub-region of the cohort stopped accumulating clinical malaria episodes earlier than other children in the study. Despite lack of further clinical episodes of malaria, these children had higher asymptomatic parasite densities and higher antibody titres to a panel of P. falciparum blood-stage antigens. Conclusions: This suggests development of clinical immunity rather than lack of exposure to the parasite, and supports the view that this immunity to malaria disease is maintained by a greater exposure to P. falciparum, and thus higher parasite burdens. Our study illustrates the complexity of anti-malaria immunity and underscores the need for analyses which can sufficiently reflect the heterogeneity within endemic populations.


Parasitology ◽  
1998 ◽  
Vol 116 (6) ◽  
pp. 501-510 ◽  
Author(s):  
C. ROPER ◽  
W. RICHARDSON ◽  
I. M. ELHASSAN ◽  
H. GIHA ◽  
L. HVIID ◽  
...  

Residents of Daraweesh village in Sudan were monitored for Plasmodium falciparum infection and malaria morbidity in 3 malaria seasons from 1993 to 1996. Malaria parasites were detected microscopically and by polymerase chain reaction (PCR) in a series of cross-sectional surveys. PCR revealed submicroscopical infections during the dry season, particularly among individuals who had recovered from a malaria episode following successful drug treatment. Clinical and subclinical infections were contrasted by assaying for allelic polymorphism at 2 gene loci, MSP-1 and GLURP and 2 hypotheses examined with reference to these data: that clinical malaria is associated with infection with novel parasite genotypes not previously detected in that host, or alternatively, that clinical malaria episodes are associated with an increased number of clones in an infection. We detected more mixed infections among clinical isolates, but people carrying parasites during the dry season were not found to have an increased risk of disease in the following malaria season. There was a clear association of disease with the appearance of novel parasite genotypes.


2013 ◽  
Vol 5 (4) ◽  
pp. 131 ◽  
Author(s):  
LyticiaA Ochola ◽  
BartholomewN Ondigo ◽  
GideonM Ng′wena ◽  
GregoryS Noland ◽  
George Ayodo ◽  
...  

2014 ◽  
Vol 58 (10) ◽  
pp. 5831-5840 ◽  
Author(s):  
Charlotte A. Lanteri ◽  
Suwanna Chaorattanakawee ◽  
Chanthap Lon ◽  
David L. Saunders ◽  
Wiriya Rutvisuttinunt ◽  
...  

ABSTRACTNovel synthetic endoperoxides are being evaluated as new components of artemisinin combination therapies (ACTs) to treat artemisinin-resistantPlasmodium falciparummalaria. We conducted blindedex vivoactivity testing of fully synthetic (OZ78 and OZ277) and semisynthetic (artemisone, artemiside, artesunate, and dihydroartemisinin) endoperoxides in the histidine-rich protein 2 enzyme-linked immunosorbent assay against 200P. falciparumisolates from areas of artemisinin-resistant malaria in western and northern Cambodia in 2009 and 2010. The order of potency and geometric mean (GM) 50% inhibitory concentrations (IC50s) were as follows: artemisone (2.40 nM) > artesunate (8.49 nM) > dihydroartemisinin (11.26 nM) > artemiside (15.28 nM) > OZ277 (31.25 nM) > OZ78 (755.27 nM).Ex vivoactivities of test endoperoxides positively correlated with dihydroartemisinin and artesunate. The isolates were over 2-fold less susceptible to dihydroartemisinin than the artemisinin-sensitiveP. falciparumW2 clone and showed sensitivity comparable to those with test endoperoxides and artesunate, with isolate/W2 IC50susceptibility ratios of <2.0. All isolates hadP. falciparumchloroquine resistance transporter mutations, with negative correlations in sensitivity to endoperoxides and chloroquine. The activities of endoperoxides (artesunate, dihydroartemisinin, OZ277, and artemisone) significantly correlated with that of the ACT partner drug, mefloquine. Isolates had mutations associated with clinical resistance to mefloquine, with 35% prevalence ofP. falciparummultidrug resistance gene 1 (pfmdr1) amplification and 84.5% occurrence of thepfmdr1Y184F mutation. GM IC50s for mefloquine, lumefantrine, and endoperoxides (artesunate, dihydroartemisinin, OZ277, OZ78, and artemisone) correlated withpfmdr1copy number. Given that current ACTs are failing potentially from reduced sensitivity to artemisinins and partner drugs, newly identified mutations associated with artemisinin resistance reported in the literature andpfmdr1mutations should be examined for their combined contributions to emerging ACT resistance.


1996 ◽  
Vol 54 (6) ◽  
pp. 632-643 ◽  
Author(s):  
Hugues Contamin ◽  
Lassana Konate ◽  
Jean-Francois Trape ◽  
Odile Mercereau-Puijalon ◽  
Christophe Rogier ◽  
...  

2001 ◽  
Vol 69 (6) ◽  
pp. 3713-3718 ◽  
Author(s):  
Daniel Dodoo ◽  
Trine Staalsoe ◽  
Haider Giha ◽  
Jørgen A. L. Kurtzhals ◽  
Bartholomew D. Akanmori ◽  
...  

ABSTRACT Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is a variant antigen expressed on the surface of infected erythrocytes. Each parasite genome contains about 40 PfEMP1 genes, but only 1 PfEMP1 gene is expressed at a given time. PfEMP1 serves as a parasite-sequestering ligand to endothelial cells and enables the parasites to avoid splenic passage. PfEMP1 antibodies may protect from disease by inhibiting sequestration, thus facilitating the destruction of infected erythrocytes in the spleen. In this study, we have measured antibodies in Ghanaian children to a conserved region of PfEMP1 by enzyme-linked immunosorbent assay and antibodies to variant molecules on erythrocytes infected with field isolates of P. falciparum by flow cytometry. Based on close clinical monitoring, the children were grouped into those who did (susceptible) and those who did not (protected) have malaria during the season. The prevalences of antibodies to both the conserved PfEMP1 peptide and the variant epitopes were greater than 50%, and the levels of immunoglobulin G (IgG) correlated with age. The levels of antibodies to both the conserved peptide and the variant epitopes were higher in protected than in susceptible children. After correcting for the effect of age, the levels of IgG to variant antigens on a Sudanese and a Ghanaian parasite isolate remained significantly higher in protected than in susceptible children. Thus, the levels of IgG to variant antigens expressed on the surface of infected erythrocytes correlated with protection from clinical malaria. In contrast, the levels of IgG to a peptide derived from a conserved part of PfEMP1 did not correlate with protection from malaria.


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