Staphylococcus aureus targets the Duffy antigen receptor for chemokines (DARC) to lyse erythrocytes
By A. Spaan, Tamara Reyes-Robles, C. Badiou, S. Cochet, K. M. Boguslawski, Pauline Yoong, C. Day, C. D. de Haas, K. V. van Kessel, F. Vandenesch and 6 more. 2015
113 citations recorded by the source corpus.
SUMMARY In order for Staphylococcus aureus to thrive inside the mammalian host, the bacterium has to overcome iron scarcity. S. aureus is thought to produce toxins that lyse erythrocytes, releasing hemoglobin, the most abundant iron source in mammals. Here we identify the Duffy antigen receptor for chemokines (DARC) as the receptor for the S. aureus hemolytic leukocidins LukED and HlgAB. By assessing human erythrocytes with DARC polymorphisms, we determined that HlgAB and LukED-mediated lysis directly relates to DARC expression. DARC is required for S. aureus-mediated lysis of human erythrocytes and DARC overexpression is sufficient to render cells susceptible to toxin-mediated lysis. HlgA and LukE bind directly to DARC through different regions, and by targeting DARC, HlgAB and LukED support S. aureus growth in a hemoglobin acquisition-dependent manner. These findings elucidate how S. aureus targets and lyses erythrocytes to release one of the scarcest nutrients within the mammalian host.
Subfields: Immunology, Molecular Biology, Physiology
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Citations in the corpus
- Staphylococcus aureus leukocidins target endothelial DARC to cause lethality in mice (2019, background): “, 1975), and the LukED and HlgAB leukocidins (Spaan et al., 2015).”
- Identification of a domain critical for Staphylococcus aureus LukED receptor targeting and lysis of erythrocytes (2020, methodology): “aureus accomplishes this by secreting LukED and HlgAB to lyse erythrocytes and access heme iron (9, 19).”