Heavy metal removal using SnO2 nanoparticles prepared in a grape extract media

SnO2 nanoparticles were first synthesized using a grape extract media, then characterized by XRD, FE-SEM, TEM, BET, and DLS techniques, and finally used as an efficient adsorbent for the removal of Pb2+ and Cd2+ ions from wastewater. The prepared sample had a tetragonal phase with an average crystallite size of 41 nm (XRD analysis), a specific surface area of 47.08 m2.g-1 (BET method)/46.25 m2.g-1 (BJH method), and a pore diameter of 6.49 nm (BJH method). The best conditions for adsorbing were a 30 ppm concentration of metal ions, ambient temperature, pH of 6, and 0.025 g of an adsorbent. The maximum adsorption for Pb and Cd ions was 97 and 93%, respectively. The Elovich model was matched as the most suitable kinetic model, indicating that the adsorption mechanism is chemical adsorption. The negative values of ΔG (Pb: -6.38 kJ.mol-1; Cd: -4.16 kJ.mol-1) represent the spontaneousness of the adsorption process. The negative values of the parameters ΔH (Pb: -63.0 kJ.mol-1; Cd: -42.95  kJ.mol-1) and ΔS (Pb: -188.8 J.mol-1; Cd: -128.4 J.mol-1) represent the exothermic nature of the adsorption

Interleukin-27 exhibited anti-inflammatory activity during Plasmodium berghei infection in mice

Interleukin-27 (IL-27) has a pleiotropic role either as a pro-inflammatory or anti-inflammatory cytokine in inflammatory related diseases. The role and involvement of IL-27 during malaria was investigated and the effects of modulating its release on the production of major inflammatory cytokines and the histopathological consequences in major affected organs during the infection were evaluated. Results showed that IL-27 concentration was significantly elevated throughout the infection but no positive correlation with the parasitaemia development observed. Augmentation of IL-27 significantly elevated the release of anti-inflammatory cytokine, IL-10 whereas antagonising and neutralising IL-27 produced the opposite. A significant elevation of pro-inflammatory cytokines (IFN-γ and IL-6) was also observed, both during augmentation and inhibition of IL-27. Thus, it is suggested that IL-27 exerts an anti-inflammatory activity in the Th1 type response by signalling the production of IL-10 during malaria. Histopathological examination showed sequestration of PRBC in the microvasculature of major organs in malarial mice. Other significant histopathological changes include hyperplasia and hypertrophy of the Kupffer cells in the liver, hyaline membrane formation in lung tissue, enlargement of the white and red pulp followed by the disappearance of germinal centre of the spleen, and tubular vacuolation of the kidney tissues. In conclusion, it is suggested that IL-27 may possibly acts as an anti-inflammatory cytokine during the infection. Modulation of its release produced a positive impact on inflammatory cytokine production during the infection, suggesting its potential in malaria immunotherapy, in which the host may benefit from its inhibition

Understanding innate immunity to Plasmodium falciparum malaria

© 2018 Dr. Marzieh JabbarzareThe malaria parasite Plasmodium falciparum still causes an incredibly high number of deaths in young children under the age of five and pregnant women annually. The pathogenesis of human malaria is due to a combination of several parasite and host factors that simultaneously influence the severity and outcome of disease. Thus, a better understanding of the roles played by innate immune cells in both pregnancy and non-pregnancy related malaria infection is crucial. In Aim 1, an in vitro model of human peripheral blood mononuclear cells (PBMCs) derived from non-immune individuals were exposed to infected erythrocytes (IEs) expressing different P. falciparum erythrocyte membrane protein 1 (PfEMP1) binding phenotypes. This included IT parasites lines (CS2, a placental parasite line expressing VAR2CSA which binds to chondroitin sulfate A (CSA) and E8B (CD36 binding)) and NF54 lines (3C (non-CD36 binding) and 3D7 (CD36 binding)). The objectives were to identify whether PfEMP1 binding phenotypes influence PBMCs cytokine response, and also to determine whether CD36 binding is parasite characteristic that influences the innate immune response. Higher cytokines secretions were observed when PBMCs were stimulated with non-CD36 binding IEs in comparison with CD36 binding IEs. Furthermore, γδ T cells represented the predominant source of IFNγ in PBMCs from naïve donors stimulated with P. falciparum IEs. The focus of Aim 2 was to investigate the ability of purified in vitro expanded γδ T cells to produce cytokines when exposed to P. falciparum IEs with different variant surface antigens. It was found that these cells can be directly activated by P. falciparum IEs. Furthermore, cytokine secretion was not substantially different in response to parasite lines expressing different PfEMP1 types. Moreover, the contribution of Vδ2+ γδ T cells to the production of IFNγ was significantly higher than that of Vδ2- γδ T cells. Nonetheless, the activation of Vδ2- γδ T cells represented an unanticipated and intriguing result in the present study. Examining the culture of Vδ2 depleted γδ T cells, a significant ability of them to produce cytokines (IFNγ, GMCSF and TNFα) was observed following exposure to P. falciparum IEs. Furthermore, activation of these cells by P. falciparum IEs for IFNγ production was highly dependent on the direct contact between the cells and the whole IEs. This activation was shown to be sensitive to trypsin digestion but not lack of expression of PfEMP1. Considering both complete and Vδ2 depleted γδ T cell cultures, it was found that the activation modes of γδ T cells subsets appeared to be different in presence or absence of Vδ2. Two different mechanisms of activation of Vδ1 and Vδ1-Vδ2- γδ T cell subsets in presence or absence of Vδ2 γδ T cells were also proposed in this study. The goal of Aim 3 was to assess the effect of various factors such as active malaria infection, life time malaria exposure and gravidity on the maternal innate immune responses. PBMCs derived from Papua New Guinea (PNG) (highly endemic area) pregnant women with and without current malaria infection and Melbourne pregnant women (non-endemic area) were exposed to P. falciparum CS2-IEs for 24 hours. The present study found that among PBMCs derived from PNG pregnant women, presence of microscopic malaria infection did not alter either secretion of IFNγ or proportion of innate immune cells positive for induction of IFNγ. With regard to malaria exposure, a significant increase in IFNγ production was observed in response to both P. falciparum CS2-IEs and Phytohaemagglutinin (PHA) in PNG samples compared to Melbourne samples. This observation was shown to be associated with significantly more active natural killer cells (NK cells) in pregnant women living in PNG. Considering the effect of gravidity, a significant elevation of IFNγ secretion in multigravidae group was observed compared to primigravidae group in PNG pregnant women (a similar, non-significant trend in Melbourne pregnant women) in response to P. falciparum CS2-IEs. This observation could be explained by the observed percentages of IFNγ producing γδ T cells and specially their Vδ2 subset being substantially higher in multigravidae women compared to primigravid women in PNG group. Together, these results suggested that the combination of exposure, not entirely specific to malaria, and gravidity significantly impacts innate immune response in pregnant women. The outcomes of these studies led to new insights that might contribute to development of new strategies in modulating the innate immune system and particularly to increasing proportions of IFNγ producing γδ T cells to safely prevent or diminish P. falciparum-induced immunopathology

Effects of interleukin-18 modulation on the pathogenesis of malaria infection

Malaria is an important parasitic infectious disease that afflicts mankind globally. The involvements of cytokines in the pathogenesis of malaria have well been documented and it has also been widely accepted that pro-inflammatory cytokines release plays crucial roles in the progression of severe pathology in malaria. Interleukin 18 (IL-18) is an important mediator which functions as an immune regulator and inducer of pro-inflammatory cytokines release. Activation of IL-18 in the immune system has been shown to amplify inflammatory responses in many disease conditions and may play a crucial role in the development of certain disease. This study is designed to determine the role and involvement of IL-18 during malaria infection and the effects of modulating its release on the course of the infection, the release of major pro- and anti-inflammatory cytokines and also the histopathological consequences in major affected organs during the infection. Male ICR mice infected with Plasmodium berghei (P. berghei) ANKA were used as malaria model in this study. Mice were injected intraperitoneally with 2 x 107 infected red blood cells. Plasma IL-18 concentrations in malaria-infected mice as measured by ELISA method, showed continuous increment from the beginning to the end of the infection. Release phase was found to be dependent on the level of severity of the infection. Modulation of the release of IL-18 was carried out by treating the malaria infected mice with recombinant mouse IL-18 (rmIL-18) and recombinant mouse IL-18 Fc chimera (rmIL-18 Fc chimera) intravenously. Inhibition of IL-18 release by rmIL-18 Fc chimera have delayed the emergence of the physical signs of infection and the development of parasitemia, subsequently prolonging the life span of mice infected with malaria. Augmentation of systemic IL-18 with rmIL-18 significantly decreased the release of anti-inflammatory cytokine (IL-10), whereas, inhibition of IL-18 with rmIL-18 Fc chimera showed increased level of IL-10. A significant elevation of pro-inflammatory cytokines (TNFα, IFNƴ, IL-1α and IL-6) was also observed during augmentation of IL-18 level. Nonetheless, these pro-inflammatory cytokines decreased during inhibition of IL-18 by rmIL-18 Fc chimera. From the pattern of cytokines release, it can be suggested that IL-18 exerts a pro-inflammatory activity in the Th1 type response by signaling the production of IFNƴ during malaria. Histopathological analysis performed on major organs known to be affected during malaria infection which include the brain, lungs, liver, spleen and kidneys of malarial mice showed significant histopathological changes in all organs of malarial mice. Treatment with rmIL-18 Fc chimera showed significant improvement on the histopathological conditions of the organs as compared to the malarial mice treated with PBS. However, mice treated with recombinant mouse IL-18 showed severe and worsening histopathology during the infection. In conclusion, the results from this study suggest that IL-18 may well play a crucial role in mediating the severity of malaria infection and it may play a key pro-inflammatory role throughout immune response against the disease. Antagonizing IL-18 activity has improved the histopathological conditions associated with the disease which may well suggest that targetting IL-18 would provide a potentially significant therapeutic benefit in malaria therapy

Innate immune responses to malaria-infected erythrocytes in pregnant women: Effects of gravidity, malaria infection, and geographic location

BACKGROUND: Malaria in pregnancy causes maternal, fetal and neonatal morbidity and mortality, and maternal innate immune responses are implicated in pathogenesis of these complications. The effects of malaria exposure and obstetric and demographic factors on the early maternal immune response are poorly understood. METHODS: Peripheral blood mononuclear cell responses to Plasmodium falciparum-infected erythrocytes and phytohemagglutinin were compared between pregnant women from Papua New Guinea (malaria-exposed) with and without current malaria infection and from Australia (unexposed). Elicited levels of inflammatory cytokines at 48 h and 24 h (interferon γ, IFN-γ only) and the cellular sources of IFN-γ were analysed. RESULTS: Among Papua New Guinean women, microscopic malaria at enrolment did not alter peripheral blood mononuclear cell responses. Compared to samples from Australia, cells from Papua New Guinean women secreted more inflammatory cytokines tumor necrosis factor-α, interleukin 1β, interleukin 6 and IFN-γ; p<0.001 for all assays, and more natural killer cells produced IFN-γ in response to infected erythrocytes and phytohemagglutinin. In both populations, cytokine responses were not affected by gravidity, except that in the Papua New Guinean cohort multigravid women had higher IFN-γ secretion at 24 h (p = 0.029) and an increased proportion of IFN-γ+ Vδ2 γδ T cells (p = 0.003). Cytokine levels elicited by a pregnancy malaria-specific CSA binding parasite line, CS2, were broadly similar to those elicited by CD36-binding line P6A1. CONCLUSIONS: Geographic location and, to some extent, gravidity influence maternal innate immunity to malaria

Fabrication, degradation behavior and cytotoxicity of nanostructured hardystonite and titania/hardystonite coatings on Mg alloys

In this study, nanostructured hardystonite (HT) and titania (TiO2)/hardystonite (HT) dual-layered coatings were deposited on biodegradable Mg-Ca-Zn alloy via physical vapor deposition (PVD) combined with electrophoretic deposition (EPD). Although a single layer nano-HT coating can decrease the corrosion rate from 1.68 to 1.02 mm/year, due to the presence of porosities and microcracks, the nano-HT layer cannot sufficiently protect the Mg substrate. In contrast, the corrosion resistance of nano-HT coating is further improved by using nano-TiO2 underlayer since it was a smooth, very uniform and compact layer with higher contact angle (52.30°). In addition, the MTT assay showed the viability of MC3T3-E1 on the nano-HT and nano-TiO2/HT coatings. The results demonstrated that the two-step surface modification improved both corrosion resistance and the cytocompatibility of the Mg alloy, hence making it feasible for orthopedic applications

Microstructure, in vitro corrosion behavior and cytotoxicity of biodegradable Mg-Ca-Zn and Mg-Ca-Zn-Bi alloys

The effects of bismuth (Bi) addition on the microstructure and corrosion behavior of the Mg-Ca-Zn-Bi alloys were evaluated using electron microscopy, electrochemical test and electrochemical impedance spectroscopy. Microstructural observations showed that Mg-1.2Ca-1Zn-xBi (x = 0.5, 1.5, 3 wt.%) are composed of Mg2Ca, Ca2Mg6Zn3 and Mg3Bi2 phases while a new phase Mg2Bi2Ca appeared after the addition of 5 and 12 wt.% Bi to the Mg-1.2Ca-1Zn alloy. Furthermore, the additions of 0.5 wt.% Bi to the Mg-1.2Ca-1Zn alloy slightly improved the corrosion behavior of the alloy, while further increase in Bi amount from 1.5 to 12 wt.% has a deleterious effect on the corrosion behavior of the ternary Mg-1.2Ca-1Zn alloy which is driven by galvanic coupling effect. Cytotoxicity tests indicate that the Mg-1.2Ca-1Zn presents higher cell viability compared to Mg-1.2Ca-1Zn-0.5Bi alloy. In addition, the cell viability of both alloys increased with increasing incubation time while diluting the extracts to 50% and 10% improved the cell viabilities. The present results suggest that the Mg-1.2Ca-1Zn-0.5Bi can be interesting candidate for the development of degradable biomaterials and it is worthwhile for further investigation in an in vivo environment

Deposition of nanostructured fluorine-doped hydroxyapatite-polycaprolactone duplex coating to enhance the mechanical properties and corrosion resistance of Mg alloy for biomedical applications

The present study addressed the synthesis of a bi-layered nanostructured fluorine-doped hydroxyapatite (nFHA)/polycaprolactone (PCL) coating on Mg-2Zn-3Ce alloy via a combination of electrodeposition (ED) and dip-coating methods. The nFHA/PCL composite coating is composed of a thick (70-80 μm) and porous layer of PCL that uniformly covered the thin nFHA film (8-10 μm) with nanoneedle-like microstructure and crystallite size of around 70-90 nm. Electrochemical measurements showed that the nFHA/PCL composite coating presented a high corrosion resistance (Rp = 2.9 × 103 kΩ cm2) and provided sufficient protection for a Mg substrate against galvanic corrosion. The mechanical integrity of the nFHA/PCL composite coatings immersed in SBF for 10 days showed higher compressive strength (34% higher) compared with the uncoated samples, indicating that composite coatings can delay the loss of compressive strength of the Mg alloy. The nFHA/PCL coating indicted better bonding strength (6.9 MPa) compared to PCL coating (2.2 MPa). Immersion tests showed that nFHA/PCL composite-coated alloy experienced much milder corrosion attack and more nucleation sites for apatite compared with the PCL coated and uncoated samples. The bi-layered nFHA/PCL coating can be a good alternative method for the control of corrosion degradation of biodegradable Mg alloy for implant applications

Microstructural, mechanical properties and corrosion behavior of plasma sprayed NiCrAlY/nano-YSZ duplex coating on Mg-1.2Ca-3Zn alloy

In this study, microstructural evolution, mechanical properties and corrosion behavior of plasma sprayed NiCrAlY/nano-yttria stabilized zirconia (nano-YSZ) dual-layered coating on Mg-1.2Ca-3Zn alloy were investigated. NiCrAlY underlayer is composed of large amount of porosities and micro-cracks with thickness around 80-90 µm. However, nano-YSZ overlayer shows bimodal microstructure consisting of columnar grains and some partially molten parts of the nanostructured powders with thickness around 270-300 µm. The microhardness of dual-layered NiCrAlY/nano-YSZ coating is significantly higher than that of single-layered NiCrAlY. Despite that, the bonding strength of dual-layered coating is slightly higher than single-layered plasma sprayed coating. Results also showed that both single-layer NiCrAlY and dual-layer NiCrAlY/nano-YSZ coatings decreased the corrosion current density of Mg alloy from 217.1 µA/cm2 to 114.5 and 82.4 µA/cm2, respectively