CCR5 is a receptor for Staphylococcus aureus leukotoxin ED

Francis Alonzo, Lina Kozhaya, Stephen A. Rawlings, Tamara Reyes-Robles, Ashley L. DuMont, David G. Myszka, Nathaniel R. Landau, Derya Unutmaz () and Victor J. Torres ()
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Francis Alonzo: New York University School of Medicine
Lina Kozhaya: New York University School of Medicine
Stephen A. Rawlings: New York University School of Medicine
Tamara Reyes-Robles: New York University School of Medicine
Ashley L. DuMont: New York University School of Medicine
David G. Myszka: Biosensor Tools LLC
Nathaniel R. Landau: New York University School of Medicine
Derya Unutmaz: New York University School of Medicine
Victor J. Torres: New York University School of Medicine

Nature, 2013, vol. 493, issue 7430, 51-55

Abstract: Abstract Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor CCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5+ leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.

Date: 2013
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DOI: 10.1038/nature11724

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