Platelet reactions after interaction with cultured Plasmodium falciparum infected erythrocytes

Inyang, A. L.; Sodeinde, Olugbemiro; Okpako, D.T.; Essien, E M

doi:10.1111/j.1365-2141.1987.tb06926.x

Cited by 20 publications

(15 citation statements)

References 11 publications

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“…Whether a systemic activation of circulating platelets occur in malaria is still unclear. While a study has reported altered platelet responses after exposure to P. falciparum infected erythrocytes (P-IE) in vitro (22), direct assessment of platelet activation through flow cytometry has rendered negative results (10, 23). However, evidence of some grade of platelet activation in vivo , through measurement of circulating factors, have been shown by other groups (5, 24).…”

Section: Discussionmentioning

confidence: 99%

Platelet disturbances correlate with endothelial cell activation in uncomplicated Plasmodium vivax malaria

Dos-Santos

Silva‐Filho

Judice

et al. 2019

Preprint

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23Introduction. Platelets drive endothelial cell activation in many diseases. 24 However, if this occurs in Plasmodium vivax malaria is unclear. As platelets have 25 been reported to be activated and to play a role in inflammatory response during 26 malaria, we hypothesized that this would correlate with endothelial alterations 27 during acute illness. 28Methods. We performed platelet flow cytometry of PAC-1 and P-selectin. We 29 measured Platelet markers (CXCL4, CD40L, P-selectin, Thrombopoietin, IL-11) and 30 endothelial markers (ICAM-1, von Willebrand Factor and E-selectin) in plasma with a 31 multiplex-based assay. The values of each mediator were used to generate heatmaps, K-32 means clustering and Principal Component analysis. In addition, we determined pair-wise 33 Pearson's correlation coefficients to generate correlation networks. 34 Results. Platelet counts were reduced, and mean platelet volume increased in 35 malaria patients. The activation of circulating platelets in flow cytometry did not differ 36 between patients and controls. CD40L levels (Median [IQ]: 517 [406-651] vs. 1029 [732-37 1267] pg/mL, P=0.0001) were significantly higher in patients, while P-selectin (Median 38 [IQ]: 17.0 [15.4-20.6] vs. 22.2 [17.6-25.7] ng/mL, P=0.0621) and CXCL4 showed a 39 nonsignificant trend towards higher levels in patients. The network correlation 40 approach demonstrated the correlation between markers of platelet and endothelial 41 activation, and the heatmaps revealed a distinct pattern of activation in two subsets 42 of P. vivax patients when compared to controls.43 Conclusion. platelet activation occurs in uncomplicated vivax malaria and 44 this correlates with higher endothelial cell activation, especially in a subset of 45 patients. 46 47 131 (R&D Systems): CD40L, P-selectin, PF4 and thrombopoietin (TPO), IL-11, as 132 well as circulating markers of EC activation (ICAM-1, E-selectin, von Willebrand 133Factor (vWF)). We selected 31 patients for the multiplex assay from a wide range 134 of parasitemias (260 to 25,150 Pv-IE/μL), so that a wide spectrum of disease 135 burden could be evaluated. This subgroup did not differ from the overall 136 population of patients regarding severity of disease, sex proportion, platelet counts 137 and mean parasitemia. We selected nine controls matched for age and sex. For the 138 network analysis, we used some interpolated results from below standard range. 139 140

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Section: Discussionmentioning

confidence: 99%

Platelet disturbances correlate with endothelial cell activation in uncomplicated Plasmodium vivax malaria

Dos-Santos

Silva‐Filho

Judice

et al. 2019

Preprint

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“…26 Additionally, humans infected with the parasite Trypanosoma cruzi and other infectious agents suffer from severe thrombocytopenia due to mobilization of sialic acid from the circulating platelets. [27][28][29] In preliminary experiments, we have found that removal of the external domain of GP1b␣ carrying complex type N-linked glycans from the platelet surface by O-sialoglycoprotein endopeptidase decreased the clearance rate of transfused platelets stored at 4°C for 24 hours (data not shown). This may suggest that domains or glycans on the external part of GP1b␣ are important for the clearance of long-term 4°C-stored platelets.…”

Section: Discussionmentioning

confidence: 99%

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Wandall

Hoffmeister

Sørensen

et al. 2008

Blood

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Cold storage of platelets for transfusion is desirable to extend platelet storage times and to prevent bacterial growth. However, the rapid clearance of coldstored platelets prevents their use. A novel method for preventing the rapid clearance of cold-stored platelets has previously been developed in a murine model. Cold storage induces the clustering and recognition of exposed ␤-Nacetylglucosamine (␤GlcNAc) on platelet surfaces. Glycosylation of ␤GlcNAc residues with uridine 5-diphosphogalactose (UDP-galactose) results in the normal survival of short-term (2 h) 0°C-stored murine platelets. Based on this finding, we developed a similar glycosylation process by adding UDP-galactose to human apheresis platelets. A phase 1 clinical trial was conducted transfusing radiolabeled autologous apheresis platelets stored for 48 hours at 4°C with or without pretreatment with UDP-galactose. In contrast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet clearance routinely observed after 4°C storage. We next developed a murine model of platelet storage for 48 hours at 4°C and showed that UDP-galactose treatment of murine platelets also did not prevent their rapid clearance, in agreement with the human platelet study. We conclude that different mechanisms of clearance may exist for short-and long-term cold-stored platelets. (Blood. 2008;111:3249-3256)

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“…Maximum induction ofADP-induced platelet aggregation was found in P. falciparum infection as compared to P. vivax malaria which reflects the vulnerability of these patients to develop platelet aggregation induced complications and endothelial injury evidenced by establishment of significant negative correlation between ADP induced platelet aggregation and hemoglobin concentration (r = -0.637) ( Figure 2). Inyang et al (19) allowed the interaction of normal platelets with R falciparum and found significant increase in aggregation response of the platelets to external stimuli such as ADP, which exhibits the platelet dysfunction. Another reason behind the increased platelet aggregation in malaria patients might be upsurged lipid peroxidation.…”

Section: I) Alterations In Hematological Parametersmentioning

confidence: 99%

Studies on biochemical changes with special reference to oxidant and antioxidants in malaria patients

Kulkarni

Suryakar

Sardeshmukh

et al. 2003

Indian J Clin Biochem

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Oxidative stress plays an important role in the development of maladal anemia. The present study was undertaken to study the role of oxidant and antioxidants in the patients of Plasmodium falciparum malada (n = 25), Plasmodium vivax malada (n = 25) as against the normal control subjects (n =25). The parameters included are the hematological [hemoglobin, erythrocyte adenosine deaminase (ADA) activity, ADP -induced platelet aggregation] and serum total lipid peroxide as an index of oxidative stress and antioxidants [erythrocytic superoxide dismutase (SOD) activity, serum vitamin E] & serum iron.Significant alterations in all above parameters were noted in both groups of malaria patients as compared to control subjects. Maximum significant alterations in hematological parameters were noticed in P. falciparum infection as compared to P. vivax malada (p<0.001). Substantial dse in serum total lipid peroxides and a significant reduction in antioxidants such as serum vitamin E and serum iron were noted in R falciparum malaria as compared to R vivax malada (p< 0.001), whereas maximum decline in erythrocytic SOD activity was observed in R vivax infection as compared to R falciparum malaria (p<0.05). Follow-up examination revealed the restoration of the levels of all biochemical parameters to the normal level after 20 days of antimalarial therapy.The study specified severity of P. falciparum malaria and also functional duality of oxidant.

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Platelet reactions after interaction with cultured Plasmodium falciparum infected erythrocytes

Cited by 20 publications

References 11 publications

Platelet disturbances correlate with endothelial cell activation in uncomplicated Plasmodium vivax malaria

Platelet disturbances correlate with endothelial cell activation in uncomplicated Plasmodium vivax malaria

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Studies on biochemical changes with special reference to oxidant and antioxidants in malaria patients

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