Evidence map›Paper›PMID 25262977›Full record

ReviewImmunology2015

Immunological mechanisms contributing to the double burden of diabetes and intracellular bacterial infections.

Kelly Hodgson, Jodie Morris, Tahnee Bridson, Brenda Govan, Catherine Rush, Natkunam Ketheesan

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed, 11 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

199 citing papers in PubMed, 11 syntheses or guidelines pooled it, 371 citations in OpenAlex.

  1. Pooled it
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  7. Diabetes and COVID-19: A systematic review on the current evidences.Diabetes research and clinical practice · 2020
    Pooled it
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  9. The double burden of diabetes and global infection in low and middle-income countries.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2019
    Pooled it
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139 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Kelly HodgsonInfectious Diseases and Immunopathogenesis Research Group, Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Qld, Australia.
Jodie Morris
Tahnee Bridson
Brenda Govan
Catherine Rush
Natkunam Ketheesan
James Cook University · AUAustralian Institute of Tropical Health and Medicine · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes has been recognized as an important risk factor for a variety of intracellular bacterial infections, but research into the dysregulated immune mechanisms contributing to the impaired host-pathogen interactions is in its infancy. Diabetes is characterized by a chronic state of low-grade inflammation due to activation of pro-inflammatory mediators and increased formation of advanced glycation end products. Increased oxidative stress also exacerbates the chronic inflammatory processes observed in diabetes. The reduced phagocytic and antibacterial activity of neutrophils and macrophages provides an intracellular niche for the pathogen to replicate. Phagocytic and antibacterial dysfunction may be mediated directly through altered glucose metabolism and oxidative stress. Furthermore, impaired activation of natural killer cells contributes to decreased levels of interferon-γ, required for promoting macrophage antibacterial mechanisms. Together with impaired dendritic cell function, this impedes timely activation of adaptive immune responses. Increased intracellular oxidation of antigen-presenting cells in individuals with diabetes alters the cytokine profile generated and the subsequent balance of T-cell immunity. The establishment of acute intracellular bacterial infections in the diabetic host is associated with impaired T-cell-mediated immune responses. Concomitant to the greater intracellular bacterial burden and potential cumulative effect of chronic inflammatory processes, late hyper-inflammatory cytokine responses are often observed in individuals with diabetes, contributing to systemic pathology. The convergence of intracellular bacterial infections and diabetes poses new challenges for immunologists, providing the impetus for multidisciplinary research.

Indexed as

Bacterial InfectionsDendritic CellsDiabetes MellitusGlycation End Products, AdvancedHumansImmunity, ActiveInflammationInterferon-gammaKiller Cells, NaturalMacrophagesNeutrophilsOxidative StressPhagocytosisRisk FactorsT-LymphocytesGlycation End Products, AdvancedInterferon-gammacell-mediated immunitydiabetesinflammationintracellular bacterial infectionsmelioidosistuberculosis

Identifiers

PMID25262977
PMCPMC4298412
OpenAlexW2023419926

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.