Nitric oxide in Tanzanian children with malaria: inverse relationship between malaria severity and nitric oxide production/nitric oxide synthase type 2 expression
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Date
1996
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Publisher
The Journal of experimental medicine
Abstract
Summary
Nitric oxide (NO)-related activity has been shown to be protective against Plasmodium faki-
parum in vitro. It has been hypothesized, however, that excess NO production contributes to the
pathogenesis of cerebral malaria. The purpose of this study was to compare markers of NO
production [urinary and plasma nitrate + nitrite (NO~)], leukocyte-inducible nitric oxide syn-
thase type 2 (NOS2), and plasma TNF-c~ and IL-10 levels with disease severity in 191 Tanza-
nian children with and without malaria. Urine NO• excretion and plasma NOx levels (cor- rected
for renal impairment) were inversely related to disease severity, with levels highest in subclinical
infection and lowest in fatal cerebral malaria. Results could not be explained by dif- ferences in
dietary nitrate ingestion among the groups. Plasma levels of IL-10, a cytokine known to suppress
NO synthesis, increased with disease severity. Leukocyte NOS2 antigen was detectable in all
control children tested and in all those with subclinical infection, but was undetectable in all but
one subject with cerebral malaria. This suppression of NO synthesis in cerebral malaria may
contribute to pathogenesis. In contrast, high fasting NO x levels and leu- kocyte NOS2 in healthy
controls and asymptomatic infection suggest that increased NO syn-thesis might protect against
clinical disease. NO appears to have a protective rather than patho-logical role in African
children with malaria.
Description
Keywords
Nitric oxide, Malaria, Tanzania
Citation
Anstey, N.M., Weinberg, J.B., Hassanali, M.Y., Mwaikambo, E.D., Manyenga, D., Misukonis, M.A., Arnelle, D.R., Hollis, D., McDonald, M.I. and Granger, D.L., 1996. Nitric oxide in Tanzanian children with malaria: inverse relationship between malaria severity and nitric oxide production/nitric oxide synthase type 2 expression. The Journal of experimental medicine, 184(2), pp.557-567.