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Sickle Hemoglobin Confers Tolerance to Plasmodium Infection

Ferreira, Ana ; Marguti, Ivo ; Bechmann, Ingo ; Jeney, Viktória ; Chora, Ângelo ; Palha, Nuno R. ; Rebelo, Sofia ; Henri, Annie ; Beuzard, Yves ; Soares, Miguel P.

Cell, 2011-04, Vol.145 (3), p.398-409 [Periódico revisado por pares]

United States: Elsevier Inc

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Título:
Sickle Hemoglobin Confers Tolerance to Plasmodium Infection
Autor: Ferreira, Ana ; Marguti, Ivo ; Bechmann, Ingo ; Jeney, Viktória ; Chora, Ângelo ; Palha, Nuno R. ; Rebelo, Sofia ; Henri, Annie ; Beuzard, Yves ; Soares, Miguel P.
Assuntos: abnormal hemoglobin ; Animals ; antigens ; carbon monoxide ; Carbon Monoxide - metabolism ; CD8-positive T-lymphocytes ; CD8-Positive T-Lymphocytes - immunology ; cerebral malaria ; Chemokines - metabolism ; Crosses, Genetic ; Disease Models, Animal ; hematopoietic stem cells ; heme ; heme oxygenase (biliverdin-producing) ; Heme Oxygenase-1 - metabolism ; Hemoglobin, Sickle - immunology ; Host-Pathogen Interactions ; Humans ; Malaria - immunology ; Malaria - physiopathology ; Malaria, Cerebral - immunology ; Malaria, Cerebral - physiopathology ; metabolism ; Mice ; Mice, Inbred C57BL ; NF-E2-Related Factor 2 - metabolism ; parasite load ; pathogenesis ; Plasmodium ; Plasmodium berghei ; protective effect ; transcription factors
É parte de: Cell, 2011-04, Vol.145 (3), p.398-409
Notas: http://dx.doi.org/10.1016/j.cell.2011.03.049
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Descrição: Sickle human hemoglobin (Hb) confers a survival advantage to individuals living in endemic areas of malaria, the disease caused by Plasmodium infection. As demonstrated hereby, mice expressing sickle Hb do not succumb to experimental cerebral malaria (ECM). This protective effect is exerted irrespectively of parasite load, revealing that sickle Hb confers host tolerance to Plasmodium infection. Sickle Hb induces the expression of heme oxygenase-1 (HO-1) in hematopoietic cells, via a mechanism involving the transcription factor NF-E2-related factor 2 (Nrf2). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after Plasmodium infection, suppressing the pathogenesis of ECM. Moreover, sickle Hb inhibits activation and/or expansion of pathogenic CD8 + T cells recognizing antigens expressed by Plasmodium, an immunoregulatory effect that does not involve Nrf2 and/or HO-1. Our findings provide insight into molecular mechanisms via which sickle Hb confers host tolerance to severe forms of malaria. [Display omitted] ► Sickle hemoglobin induces the expression of heme oxygenase-1 (HO-1) ► HO-1 produces carbon monoxide (CO), which affords protection against malaria ► CO does not modulate host parasite load ► Sickle hemoglobin confers host tolerance to malaria
Editor: United States: Elsevier Inc
Idioma: Inglês

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Sickle Hemoglobin Confers Tolerance to Plasmodium Infection

Ferreira, Ana ; Marguti, Ivo ; Bechmann, Ingo ; Jeney, Viktória ; Chora, Ângelo ; Palha, Nuno R. ; Rebelo, Sofia ; Henri, Annie ; Beuzard, Yves ; Soares, Miguel P.

United States: Elsevier Inc

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