Copper Homeostasis at the Host-Pathogen Interface
Open accessAbstract
The trace element copper is indispensable for all aerobic life forms. Its ability to cycle between two oxidation states, Cu(1+) and Cu(2+), has been harnessed by a wide array of metalloenzymes that catalyze electron transfer reactions. The metabolic needs for copper are sustained by a complex series of transporters and carrier proteins that regulate its intracellular accumulation and distribution in both pathogenic microbes and their animal hosts. However, copper is also potentially toxic due in part to its ability to generate reactive oxygen species. Recent studies suggest that the macrophage phagosome accumulates copper during bacterial infection, which may constitute an important mechanism of killing. Bacterial countermeasures include the up-regulation of copper export and detoxification genes during infection, which studies suggest are important determinants of virulence. In this minireview, we summarize recent developments that suggest an emerging role for copper as an unexpected component in determining the outcome of host-pathogen interactions.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Within macrophages, Cu accumulates in the phagolysosome of immune cells to combat infection by a defined pathway.
“Within macrophages, Cu accumulates in the phagolysosome of immune cells to combat infection by a defined pathway 149 (Fig. 5) .”
From Nutritional immunity: the battle for nutrient metals at the host–pathogen interface (2022) · cites this paper as [149]
The 'Importance of Mammalian Copper Transporters in Macrophage Bactericidal Activity' section describes ATP7A trafficking to the phagolysosome and evidence linking it to bacterial killing. Figure 1 models a copper-delivery pathway, but the 'Possible Mechanism of Copper-dependent Bacterial Killing by Macrophages' section says the killing mechanism remains unanswered. Calling the pathway by which copper combats infection 'defined' overstates the source. (LLM, conf=0.87)
Experimental — accuracy not yet measuredM. tuberculosis expresses mycobacterial copper transport protein B (MctB) and ATPase CtpV, which play an important role for pathogen proliferation by avoiding copper intoxication within the phagolysosome and maintaining low copper levels.
“On the other hand, M. tuberculosis expresses the mycobacterial copper transport protein B (MctB) and the ATPase CtpV, which play an important role for pathogen proliferation by avoiding copper intoxication within the phagolysome and maintaining low copper levels in this environment (160, 237–239).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [237]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 88 · Cited by 316
- Authors
- Hodgkinson, V., & Petris, M. J.
- Affiliations
- University of Missouri (US)
- Corresponding author
- Petris, Michael J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 287
- Issue
- 17
- Pages
- 13549-13555
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3340201
- OpenAlex
- W2060062898
- Cited by
- 316
- References
- 88
- Citations by year
- 2026: 22 · 2025: 17 · 2024: 21 · 2023: 21 · 2022: 23 · 2021: 24 · 2020: 40 · 2019: 21 · 2018: 20 · 2017: 13 · 2016: 26 · 2015: 25 · 2014: 17 · 2013: 19 · 2012: 6
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK093866, DK 59893, R01DK093866, R01DK059893)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Keywords
- copper homeostasis, host-pathogen interaction, copper transporters, copper exports, copper detoxification, reactive oxygen species, bacterial virulence, metalloenzymes, bacterial infection
- MeSH terms
- Copper-Transporting ATPases, Adenosine Triphosphatases, Anti-Bacterial Agents, Bacteria, Biological Transport, Copper, Homeostasis, Humans, Mycobacterium tuberculosis, Oxygen, Pseudomonas, Salmonella typhimurium, Trace Elements, Virulence, Reactive Oxygen Species, Cation Transport Proteins, Host-Pathogen Interactions
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
