Expression of proinflammatory cytokines in four regions of the brain in Macaque mulatta (rhesus) monkeys infected with Plasmodium coatneyi.

Tongren, Jon Eric; Yang, Chunfu; Collins, William E.; Sullivan, JoAnn S.; Lal, Altaf A.; Xiao, Lihua

doi:10.4269/ajtmh.2000.62.530

Cited by 25 publications

(15 citation statements)

References 25 publications

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“…In some reports, histopathological features found in CM in humans are associated with local production of TNF-␣, IFN-␥, and IL-1␤ but also of IL-10 (50). Similar results have been found in a monkey model of CM (95). However, other authors have found that the mRNA of proinflammatory (TNF-␣ and IL-1␤) cytokines, detected in postmortem samples of patients suffering CM, does not correlate with the density of parasitized erythrocytes.…”

Section: Cytokines In the Immunopathology Of Malariasupporting

confidence: 84%

Cytokines in the Pathogenesis of and Protection against Malaria

Angulo

Fresno

2002

Clin Vaccine Immunol

116

106

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Malaria is caused by the protozoan Plasmodium, transmitted to humans by Anopheles mosquitoes. The most dangerous of the plasmodia infecting humans is Plasmodium falciparum. Most of the clinical signs of this disease are caused by the parasite at stages in which it multiplies asexually in red blood cells. P. falciparum infection is most severe in children. However, only a small proportion of infected children develop severe complications; in nonimmune individuals these can cause severe and life-threatening disease. The reasons for these differences are not fully understood, but it is likely that host genetic, immune, and social and geographic factors play a role. Malaria is the world's most prevalent parasitic disease and against which effective control measures are urgently needed. Many attempts have been made by using several Plasmodium antigens both in model systems and in humans to develop a malaria vaccine. However, the results, although encouraging, are far from satisfactory (36, 73). One of the difficulties hindering the design of a successful vaccine against Plasmodium is our current incomplete knowledge of protective immunity and how it can be induced. Moreover, the pathogenesis of two of the most severe complications of P. falciparum malaria, cerebral malaria (CM) and severe malarial anemia (SA), both appear to involve dysregulation of the immune system (56). Therefore, a greater appreciation of the mechanisms of protective immunity on the one hand and of immunopathology on the other would provide crucial clues as to how manipulation of the immune system may best be achieved in order to reach the goal of better vaccines.The purpose of this review is to summarize recent work on the role of cytokines in antiparasitic immune responses and immunopathology caused by blood-stage parasites. Although, other points in the biological cycle of Plasmodium offer attractive sites for prophylactic intervention, all clinical symptoms are provoked by this parasitic stage.

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Section: Cytokines In the Immunopathology Of Malariasupporting

confidence: 84%

Cytokines in the Pathogenesis of and Protection against Malaria

Angulo

Fresno

2002

Clin Vaccine Immunol

116

106

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“…For each of the six antigens studied, the highest levels of expression observed were those in the sections of cerebellum from the CM cases. Similarly, the expression of cytokines (Tongren et al, 2000) and adhesion molecules (Smith et al, 1996) in rhesus monkeys infected with P. coatneyi was found to be greater in the cerebellum than any other region of the brain. The high levels of cytokine and adhesion-molecule expression in the cerebellar tissues of human cases of CM (present study) match well with the histopathological observations, made in both human CM (Sein et al, 1993a) and the rhesus-monkey model of CM (Sein et al, 1993b;Smith et al, 1996;Tongren et al, 2000), of higher levels of parasitisederythrocyte sequestration in the cerebellum than elsewhere in the brain.…”

Section: Receptormentioning

confidence: 90%

“…As, in in-vitro studies, IL-1b has been found to be neurotoxic and to be rapidly induced in response to neuronal cell death, it may play a causal role in ischaemic cell death and neurodegeneration in the brain (Rothwell and Strijbos, 1995). In samples of cerebellum from primates with malaria, whether rhesus monkeys infected with P. coatneyi or humans with CM, expression of the mRNA for the proinflammatory cytokines (IL-1b and TNF) and the Th1 cytokine IFN-c appears to peak late in the infection, at the same time as histopathological observations reveal the preferential sequestration of parasitised erythrocytes (Sein et al, 1993a, b;Smith et al, 1996;Tongren et al, 2000). Recent evidence from studies on mice indicates, however, that it may be the over-production of LT-a, rather than TNF, that leads to CM (Engwerda et al, 2002).…”

mentioning

confidence: 93%

High-level cerebellar expression of cytokines and adhesion molecules in fatal, paediatric, cerebral malaria

Armah

Dodoo

Wiredu

et al. 2005

Annals of Tropical Medicine & Parasitology

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Although the roles played by systemic tumour necrosis factor (TNF) and interleukin 1beta (IL-1beta), and their upregulation of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and E-selectin, in the pathogenesis of human cerebral malaria (CM) are well established, the role of local cytokine release, in the brain, remains unclear. Immunohistochemistry was therefore used to compare the expression of ICAM-1, VCAM-1, E-selectin, IL-1beta, TNF and transforming growth factor beta (TGF-beta) at light-microscope level, in cryostat sections of cerebral, cerebellar and brainstem tissues collected, post-mortem, from Ghanaian children. Among the 21 children investigated were 10 cases of CM, five of severe malarial anemia (SMA), one of purulent bacterial meningitis (PBM), two of non-central-nervous-system infection (NCNSI) and three children who had no infection (NI) when they died. Parasitised erythrocytes were detected in all of the sections from the cases of fatal malaria (CM and SMA), and sequestered leucocytes were present in most of the sections from the CM cases (but none of the sections from the SMA cases). Significantly elevated vascular expression of all three adhesion molecules investigated was detected in the brains of the 15 cases of fatal malaria and one of the cases of NCNSI (a child with Salmonella septicaemia), and in the malaria cases this showed highly significant co-localization with the areas of erythrocyte sequestration. In terms of the levels of expression of ICAM-1, VCAM-1 and E-selectin, there were, however, negligible differences between the CM and SMA cases. Although TGF-beta showed intravascular and perivascular distribution in all the subjects, its expression was most intense in the PBM case and the CM group. Only in the sections from the PBM and CM cases did TNF and IL-1beta show prominent brain parenchymal staining, in addition to the intravascular and perivascular staining seen in all subjects. The highest observed expression of each of the six antigens studied was in the cerebellar sections of the malaria cases. Endothelial activation in the brain therefore appears to be a feature of fatal malaria and Salmonella sepsis, and in cases of fatal malaria is closely associated with leucocyte sequestration. In the present study, IL-1beta and TNF were only up-regulated in the brains of children with neurodegenerative lesions, whereas TGF-beta was present in all cases.

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“…However, at 48 h, riluzole treatment significantly reduced the permeability in the 2 regions. Tongren et al [46] have previously shown that proinflammatory cytokine expression may differ in the brain regions during an infection. Brain may produce differential local immune response to the same infection.…”

Section: Degeneration Of Neurons (0 -3) 2 Pericellular and Vascularmentioning

confidence: 99%

The Effects of Riluzole on Neurological, Brain Biochemical, and Histological Changes in Early and Late Term of Sepsis in Rats

Toklu

Uysal

Kabasakal

et al. 2009

Journal of Surgical Research

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Expression of proinflammatory cytokines in four regions of the brain in Macaque mulatta (rhesus) monkeys infected with Plasmodium coatneyi.

Cited by 25 publications

References 25 publications

Cytokines in the Pathogenesis of and Protection against Malaria

Cytokines in the Pathogenesis of and Protection against Malaria

High-level cerebellar expression of cytokines and adhesion molecules in fatal, paediatric, cerebral malaria

The Effects of Riluzole on Neurological, Brain Biochemical, and Histological Changes in Early and Late Term of Sepsis in Rats

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