Faculty Collaboration Database

CD36 mediates the phagocytosis of Plasmodium falciparum-infected erythrocytes by rodent macrophages. J Infect Dis 2004 Jan 15;189(2):204-13

Date

01/15/2004

Pubmed ID

14722884

DOI

10.1086/380764

Scopus ID

2-s2.0-0742324946 (requires institutional sign-in at Scopus site)   114 Citations

Abstract

Phagocytic cells represent an important line of innate defense against malaria; however, little is known of the mechanism by which macrophages recognize Plasmodium falciparum-parasitized erythrocytes (PEs). Using macrophages from CD36 wild-type (WT), CD36-null, and CD36 transgenically-rescued rodents, we demonstrate a major role for CD36 in the phagocytosis of PEs. WT macrophages display enhanced phagocytic capacity for nonopsonized PEs, compared with that for CD36-null mouse and rat macrophages. Transgenic rescue of CD36-deficient rats restored macrophage phagocytic capacity for PEs. CD36 receptor blockade with monoclonal antibodies and proteolytic cleavage of CD36 ligands from the surface of PEs inhibited the uptake of PEs. Up-regulation of rodent CD36 by use of peroxisome proliferator-activated receptor (PPARgamma) agonists increased the phagocytosis of PEs. CD36-mediated uptake of PEs did not result in increased tumor necrosis factor-alpha secretion, of which high levels are associated with adverse outcomes in malaria. These studies support the use of these rodent models to examine PE-CD36 interactions.

Author List

Patel SN, Serghides L, Smith TG, Febbraio M, Silverstein RL, Kurtz TW, Pravenec M, Kain KC

Author

Roy L. Silverstein MD Professor in the Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
CD36 Antigens
Erythrocytes
Interleukin-6
Macrophages
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Phagocytosis
Plasmodium falciparum
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptors, Cytoplasmic and Nuclear
Receptors, Retinoic Acid
Retinoid X Receptors
Transcription Factors
Tumor Necrosis Factor-alpha