Degradation of endothelial glycocalyx in Tanzanian children with falciparum malaria.
endothelium
glycocalyx
glycosaminoglycans
malaria
vascular dysfunction
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
revised:
25
06
2021
received:
13
02
2021
accepted:
01
07
2021
entrez:
17
8
2021
pubmed:
18
8
2021
medline:
10
9
2021
Statut:
ppublish
Résumé
A layer of glycocalyx covers the vascular endothelium serving important protective and homeostatic functions. The objective of this study was to determine if breakdown of the endothelial glycocalyx (eGC) occurs during malaria infection in children. Measures of eGC integrity, endothelial activation, and microvascular reactivity were prospectively evaluated in 146 children: 44 with moderately severe malaria (MSM), 42 with severe malaria (SM), and 60 healthy controls (HC). Biochemical measures of eGC integrity included plasma syndecan-1 and total urinary glycosaminoglycans (GAG). Side-stream dark field imaging was used to quantitatively assess integrity of eGC. Plasma angiopoietin-2 (Ang-2) was measured as a marker of endothelial activation and also as a possible mediator of eGC breakdown. Our results show that urinary GAG, syndecan-1, and Ang-2 were elevated in patients with MSM and SM compared with HC. Syndecan-1 and GAG levels correlated significantly with each other and with plasma Ang-2. The eGC breakdown products also inversely correlated significantly with hemoglobin and platelet count. In the MSM group, imaging results provided further evidence for eGC degradation. Although not correlated with markers of eGC degradation, vascular function (assessed by non-invasive near infrared spectroscopy [NIRS]) demonstrated reduced microvascular reactivity, particularly affecting the SM group. Our findings provide further evidence for breakdown of eGC in falciparum malaria that may contribute to endothelial activation and adhesion of parasitized red blood cells, with reduced nitric oxide formation, and vascular dysfunction.
Identifiants
pubmed: 34403544
doi: 10.1096/fj.202100277RR
pmc: PMC8375618
mid: NIHMS1721347
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
e21805Subventions
Organisme : NIAID NIH HHS
ID : R34 AI100784
Pays : United States
Organisme : NIAID NIH HHS
ID : K23 AI116869
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI041764
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL130763
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI041764
Pays : United States
Informations de copyright
© 2021 Federation of American Societies for Experimental Biology.
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