Pathophysiology of Cerebral Malaria: Implications of MSCs as A Regenerative Medicinal Tool

Chaudhary, Anand Kumar; Kataria, Poonam; Surela, Neha; Das, Jyoti

doi:10.3390/bioengineering9060263

Cited by 6 publications

(6 citation statements)

References 95 publications

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“…Platelets have also been implicated in the formation of erythrocyte clumps during P. falciparum infection [ 142 ]. Infected erythrocytes can bind to platelets and the platelets function as bridges between infected erythrocytes [ 143 ].…”

Section: Cytoadherence Receptorsmentioning

confidence: 99%

Knobs, Adhesion, and Severe Falciparum Malaria

Wiser

2023

TropicalMed

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Plasmodium falciparum can cause a severe disease with high mortality. A major factor contributing to the increased virulence of P. falciparum, as compared to other human malarial parasites, is the sequestration of infected erythrocytes in the capillary beds of organs and tissues. This sequestration is due to the cytoadherence of infected erythrocytes to endothelial cells. Cytoadherence is primarily mediated by a parasite protein expressed on the surface of the infected erythrocyte called P. falciparum erythrocyte membrane protein-1 (PfEMP1). PfEMP1 is embedded in electron-dense protuberances on the surface of the infected erythrocytes called knobs. These knobs are assembled on the erythrocyte membrane via exported parasite proteins, and the knobs function as focal points for the cytoadherence of infected erythrocytes to endothelial cells. PfEMP1 is a member of the var gene family, and there are approximately 60 antigenically distinct PfEMP1 alleles per parasite genome. Var gene expression exhibits allelic exclusion, with only a single allele being expressed by an individual parasite. This results in sequential waves of antigenically distinct infected erythrocytes and this antigenic variation allows the parasite to establish long-term chronic infections. A wide range of endothelial cell receptors can bind to the various PfEMP1 alleles, and thus, antigenic variation also results in a change in the cytoadherence phenotype. The cytoadherence phenotype may result in infected erythrocytes sequestering in different tissues and this difference in sequestration may explain the wide range of possible clinical manifestations associated with severe falciparum malaria.

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Section: Cytoadherence Receptorsmentioning

confidence: 99%

Knobs, Adhesion, and Severe Falciparum Malaria

Wiser

2023

TropicalMed

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“…Salah satunya yaitu sel darah merah yang telah terinfeksi menempel pada endotelium otak menyebabkan penyumbatan di pembuluh darah sehingga jaringan di otak mengalami hipoksia dan kekurangan nutrisi. Akibat dari hal tersebut, jaringan otak tidak dapat mempertahankan potensial membran yang menyebabkan cairan masuk dari ekstraseluler ke dalam kompartemen intraseluler yang berakibat pada kematian sel dan kerusakan jaringan (Chaudhary et al, 2022).…”

Section: Patofisiologiunclassified

“…Menurut penjelasan lain, sekuestrasi sel darah merah yang terinfeksi akan meningkatkan pembentukan roset dari pengikatan sel darah merah yang terinfeksi dengan yang tidak terinfeksi (Chaudhary et al, 2022). Ketika berlangsungnya proses sekuestrasi dari sel darah merah yang terinfeksi, terjadi adhesi trombosit pada permukaan sel endotel yang menyebabkan penggumpalan dari sel darah merah.…”

Section: Patofisiologiunclassified

“…ET-1 meningkatkan rekrutmen sel darah merah terinfeksi, leukosit, dan trombosit sehingga terjadi obstruksi mikrovaskular dan vasokonstriksi. Mekanisme proinflamasi ini menyebabkan kerusakan sawar darah otak dan meningkatkan permeabilitasnya sehingga menyebabkan perdarahan dan petechiae (Chaudhary et al, 2022;Ndunge et al, 2022). Terganggunya integritas sawar darah otak dapat menyebabkan masuknya faktor plasma seperti albumin yang beracun bagi neuron (Schiess et al, 2020).…”

Section: Patofisiologiunclassified

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Cerebral Malaria

Salsabila,

Mawadddah,

Nabil

et al. 2023

JBT

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Cerebral malaria is the worst complication of malaria caused by Plasmodium spp. This disease is spread in tropical and subtropical countries and can attack all age groups and genders. The peak incidence occurs in preschool children and very often causes death in children. The endemic areas of malaria in Indonesia include NTT, Maluku, West Papua and Papua. Every year, as much as 40% of the total global population lives in or visits endemic areas every year. Cerebral malaria can cause long-term neurocognitive complications that can reduce quality of life. The speed of treatment determines the patient's prognosis. Therefore, it is necessary to understand the signs of malaria and the complications that can arise. This article was written to discuss cerebral malaria as a whole based on existing literature.

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“…CM is a fatal neurological complication of P. falciparum malaria characterized by brain tissue hemorrhages and the accumulation of infected red blood cells (iRBCs) and immune cells in brain microvessels, which can lead to blood–brain barrier (BBB) disruption and death ( 4 ). Although sequestration is thought to be the hallmark of CM, the mechanisms involved in the pathophysiology are still incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Monocytes, particularly nonclassical ones, lose their opsonic and nonopsonic phagocytosis capacity during pediatric cerebral malaria

Vianou,

Royo,

Dechavanne

et al. 2024

Front. Immunol.

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IntroductionInnate immunity is crucial to reducing parasite burden and contributing to survival in severe malaria. Monocytes are key actors in the innate response and, like macrophages, are plastic cells whose function and phenotype are regulated by the signals from the microenvironment. In the context of cerebral malaria (CM), monocyte response constitutes an important issue to understand. We previously demonstrated that decreased percentages of nonclassical monocytes were associated with death outcomes in CM children. In the current study, we postulated that monocyte phagocytosis function is impacted by the severity of malaria infection.MethodsTo study this hypothesis, we compared the opsonic and nonopsonic phagocytosis capacity of circulant monocytes from Beninese children with uncomplicated malaria (UM) and CM. For the CM group, samples were obtained at inclusion (D0) and 3 and 30 days after treatment (D3, D30). The phagocytosis capacity of monocytes and their subsets was characterized by flow cytometry and transcriptional profiling by studying genes known for their functional implication in infected-red blood cell (iRBC) elimination or immune escape.ResultsOur results confirm our hypothesis and highlight the higher capacity of nonclassical monocytes to phagocyte iRBC. We also confirm that a low number of nonclassical monocytes is associated with CM outcome when compared to UM, suggesting a mobilization of this subpopulation to the cerebral inflammatory site. Finally, our results suggest the implication of the inhibitory receptors LILRB1, LILRB2, and Tim3 in phagocytosis control.DiscussionTaken together, these data provide a better understanding of the interplay between monocytes and malaria infection in the pathogenicity of CM.

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Pathophysiology of Cerebral Malaria: Implications of MSCs as A Regenerative Medicinal Tool

Cited by 6 publications

References 95 publications

Knobs, Adhesion, and Severe Falciparum Malaria

Knobs, Adhesion, and Severe Falciparum Malaria

Cerebral Malaria

Monocytes, particularly nonclassical ones, lose their opsonic and nonopsonic phagocytosis capacity during pediatric cerebral malaria

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