An Immunohistochemical study of the pathology of fatal malaria

G. Turner, H. Morrison, M. Jones, Timothy Davis, S. Looareesuwan, I. Buley, K. Gatter, C. Newbold, S. Pukrittayakamee, B. Nagachinta, N.J. White, A. Berendt

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    Abstract

    The sequestration of parasitized erythrocytes in the microvasculature of vital organs is central to the pathogenesis of severe plasmodium falciparum malaria. This process is mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (IGAM-1) and CD36. Using immunohistochemistry we have examined the distribution of putative sequestration receptors in different organs from fatal cases of P. falciparum malaria and noninfected controls. Receptor expression and parasite sequestration in the brain were quantified and correlated. Fatal malaria was associated with widespread induction of endothelial activation markers, with significantly higher levels of ICAM-1 and E-selectin expression on vessels in the brain. In contrast cerebral endothelial CD36 and thrombospondin staining were sparse, with no evidence for increased expression in malaria There was highly significant co-localization of sequestration with the expression of ICAM-1, CD36, and E-selectin in cerebral vessels but no cellular inflammatory response. These results suggest that these receptors have a role in sequestration in vivo and indicate that systemic endothelial activation is a feature of fatal malaria.
    Original languageEnglish
    Pages (from-to)1057-1069
    JournalAmerican Journal of Pathology
    Volume145
    Publication statusPublished - 1994

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    Intercellular Adhesion Molecule-1
    Malaria
    E-Selectin
    Falciparum Malaria
    Pathology
    Parasites
    Thrombospondins
    Vascular Endothelium
    Brain
    Microvessels
    Erythrocytes
    Immunohistochemistry
    Staining and Labeling
    Ligands

    Cite this

    Turner, G., Morrison, H., Jones, M., Davis, T., Looareesuwan, S., Buley, I., ... Berendt, A. (1994). An Immunohistochemical study of the pathology of fatal malaria. American Journal of Pathology, 145, 1057-1069.
    Turner, G. ; Morrison, H. ; Jones, M. ; Davis, Timothy ; Looareesuwan, S. ; Buley, I. ; Gatter, K. ; Newbold, C. ; Pukrittayakamee, S. ; Nagachinta, B. ; White, N.J. ; Berendt, A. / An Immunohistochemical study of the pathology of fatal malaria. In: American Journal of Pathology. 1994 ; Vol. 145. pp. 1057-1069.
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    abstract = "The sequestration of parasitized erythrocytes in the microvasculature of vital organs is central to the pathogenesis of severe plasmodium falciparum malaria. This process is mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (IGAM-1) and CD36. Using immunohistochemistry we have examined the distribution of putative sequestration receptors in different organs from fatal cases of P. falciparum malaria and noninfected controls. Receptor expression and parasite sequestration in the brain were quantified and correlated. Fatal malaria was associated with widespread induction of endothelial activation markers, with significantly higher levels of ICAM-1 and E-selectin expression on vessels in the brain. In contrast cerebral endothelial CD36 and thrombospondin staining were sparse, with no evidence for increased expression in malaria There was highly significant co-localization of sequestration with the expression of ICAM-1, CD36, and E-selectin in cerebral vessels but no cellular inflammatory response. These results suggest that these receptors have a role in sequestration in vivo and indicate that systemic endothelial activation is a feature of fatal malaria.",
    author = "G. Turner and H. Morrison and M. Jones and Timothy Davis and S. Looareesuwan and I. Buley and K. Gatter and C. Newbold and S. Pukrittayakamee and B. Nagachinta and N.J. White and A. Berendt",
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    Turner, G, Morrison, H, Jones, M, Davis, T, Looareesuwan, S, Buley, I, Gatter, K, Newbold, C, Pukrittayakamee, S, Nagachinta, B, White, NJ & Berendt, A 1994, 'An Immunohistochemical study of the pathology of fatal malaria' American Journal of Pathology, vol. 145, pp. 1057-1069.

    An Immunohistochemical study of the pathology of fatal malaria. / Turner, G.; Morrison, H.; Jones, M.; Davis, Timothy; Looareesuwan, S.; Buley, I.; Gatter, K.; Newbold, C.; Pukrittayakamee, S.; Nagachinta, B.; White, N.J.; Berendt, A.

    In: American Journal of Pathology, Vol. 145, 1994, p. 1057-1069.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - An Immunohistochemical study of the pathology of fatal malaria

    AU - Turner, G.

    AU - Morrison, H.

    AU - Jones, M.

    AU - Davis, Timothy

    AU - Looareesuwan, S.

    AU - Buley, I.

    AU - Gatter, K.

    AU - Newbold, C.

    AU - Pukrittayakamee, S.

    AU - Nagachinta, B.

    AU - White, N.J.

    AU - Berendt, A.

    PY - 1994

    Y1 - 1994

    N2 - The sequestration of parasitized erythrocytes in the microvasculature of vital organs is central to the pathogenesis of severe plasmodium falciparum malaria. This process is mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (IGAM-1) and CD36. Using immunohistochemistry we have examined the distribution of putative sequestration receptors in different organs from fatal cases of P. falciparum malaria and noninfected controls. Receptor expression and parasite sequestration in the brain were quantified and correlated. Fatal malaria was associated with widespread induction of endothelial activation markers, with significantly higher levels of ICAM-1 and E-selectin expression on vessels in the brain. In contrast cerebral endothelial CD36 and thrombospondin staining were sparse, with no evidence for increased expression in malaria There was highly significant co-localization of sequestration with the expression of ICAM-1, CD36, and E-selectin in cerebral vessels but no cellular inflammatory response. These results suggest that these receptors have a role in sequestration in vivo and indicate that systemic endothelial activation is a feature of fatal malaria.

    AB - The sequestration of parasitized erythrocytes in the microvasculature of vital organs is central to the pathogenesis of severe plasmodium falciparum malaria. This process is mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (IGAM-1) and CD36. Using immunohistochemistry we have examined the distribution of putative sequestration receptors in different organs from fatal cases of P. falciparum malaria and noninfected controls. Receptor expression and parasite sequestration in the brain were quantified and correlated. Fatal malaria was associated with widespread induction of endothelial activation markers, with significantly higher levels of ICAM-1 and E-selectin expression on vessels in the brain. In contrast cerebral endothelial CD36 and thrombospondin staining were sparse, with no evidence for increased expression in malaria There was highly significant co-localization of sequestration with the expression of ICAM-1, CD36, and E-selectin in cerebral vessels but no cellular inflammatory response. These results suggest that these receptors have a role in sequestration in vivo and indicate that systemic endothelial activation is a feature of fatal malaria.

    M3 - Article

    VL - 145

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    JO - The American Journal of Pathology

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    Turner G, Morrison H, Jones M, Davis T, Looareesuwan S, Buley I et al. An Immunohistochemical study of the pathology of fatal malaria. American Journal of Pathology. 1994;145:1057-1069.