Copper redistribution in murine macrophages in response to Salmonella infection

Achard, Maud E. S., Stafford, Sian L., Bokil, Nilesh J., Chartres, Jy, Bernhardt, Paul V., Schembri, Mark A., Sweet, Matthew J. and McEwan, Alastair G. (2012) Copper redistribution in murine macrophages in response to Salmonella infection. Biochemical Journal, 444 1: 51-57. doi:10.1042/BJ20112180

Author Achard, Maud E. S.
Stafford, Sian L.
Bokil, Nilesh J.
Chartres, Jy
Bernhardt, Paul V.
Schembri, Mark A.
Sweet, Matthew J.
McEwan, Alastair G.
Title Copper redistribution in murine macrophages in response to Salmonella infection
Journal name Biochemical Journal   Check publisher's open access policy
ISSN 0264-6021
Publication date 2012-05-15
Sub-type Article (original research)
DOI 10.1042/BJ20112180
Volume 444
Issue 1
Start page 51
End page 57
Total pages 7
Place of publication London, England, U.K.
Publisher Portland Press
Collection year 2013
Language eng
Formatted abstract
The movement of key transition metal ions is recognized to be of critical importance in the interaction between macrophages and intracellular pathogens. The present study investigated the role of copper in mouse macrophage responses to Salmonella enterica sv. Typhimurium. The copper chelator BCS (bathocuproinedisulfonic acid, disodium salt) increased intracellular survival of S. Typhimurium within primary mouse BMM (bone-marrow-derived macrophages) at 24 h post-infection, implying that copper contributed to effective host defence against this pathogen. Infection of BMM with S. Typhimurium or treatment with the TLR (Toll-like receptor) 4 ligand LPS (lipopolysaccharide) induced the expression of several genes encoding proteins involved in copper transport [Ctr (copper transporter) 1, Ctr2 and Atp7a (copper-transporting ATPase 1)], as well as the multi-copper oxidase Cp (caeruloplasmin). Both LPS and infection with S. Typhimurium triggered copper accumulation within punctate intracellular vesicles (copper ‘hot spots’) in BMM as indicated by the fluorescent reporter CS1 (copper sensor 1). These copper hot spots peaked in their accumulation at approximately 18 h post-stimulation and were dependent on copper uptake into cells. Localization studies indicated that the copper hot spots were in discrete vesicles distinct from Salmonella containing vacuoles and lysosomes. We propose that copper hot spot formation contributes to antimicrobial responses against professional intracellular bacterial pathogens
Keyword Copper redistribution
Copper sensor 1 (CS1)
Innate immunity
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2013 Collection
School of Chemistry and Molecular Biosciences
Institute for Molecular Bioscience - Publications
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Citation counts: TR Web of Science Citation Count  Cited 32 times in Thomson Reuters Web of Science Article | Citations
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Created: Tue, 12 Jun 2012, 10:09:28 EST by Lucy O'Brien on behalf of School of Chemistry & Molecular Biosciences