Evidence map›Paper›PMID 24671137›Full record

ArticlePloS one2014

Phagocytosis via complement or Fc-gamma receptors is compromised in monocytes from type 2 diabetes patients with chronic hyperglycemia.

Blanca I Restrepo, Marcel Twahirwa, Mohammad H Rahbar, Larry S Schlesinger

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 122 citations in OpenAlex.

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11 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

4 authors at 3 institutions in 1 country.

Blanca I RestrepoDivision of Epidemiology, UTHealth Houston, School of Public Health at Brownsville, Brownsville, Texas, United States of America.
Marcel TwahirwaJoslin Diabetes Center-Doctors Hospital at Renaissance, Edinburg, Texas, United States of America.
Mohammad H RahbarDivision of Clinical and Translational Sciences, Department of Internal Medicine, Medical School, University of Texas Health Science Center at Houston, Houston, Texas, United States of America.
Larry S SchlesingerCenter for Microbial Interface Biology and Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, United States of America.
Joslin Diabetes Center · USThe Ohio State University · USThe University of Texas Health Science Center at Houston · US

Funding

Uncontrolled diabetes, immune dysregulation and tuberculosisR21AI079624 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI RESTREPO, BLANCA I · 2009 to 2010
$413k
NIAID NIH HHS R21 AI079624NIAID NIH HHS R21AI079624-01A1
6 · The paper itself

Abstract

Type 2 diabetes patients (DM2) have a higher risk of tuberculosis (TB) that may be attributed to functional defects in their mononuclear phagocytes given the critical role of these cells in Mycobacterium tuberculosis containment. Our previous findings suggest that monocytes from DM2 have reduced association with serum-opsonized M. tuberculosis. To determine if this alteration is due to defects in phagocytosis via complement or Fc-gamma receptors (FcγRs), in this study we evaluated the uptake of sheep red blood cells coated with IgG or complement, respectively, by monocytes from individuals with and without DM2. We found that chronic hyperglycemia was significantly associated with reduced phagocytosis via either receptor by univariable and multivariable analyses. This defect was independent of host serum opsonins and flow cytometry data indicated this was not attributed to reduced expression of these phagocytic receptors on DM2 monocytes. The positive correlation between both pathways (R = 0.64; p = 0.003) indicate that monocytes from individuals with chronic hyperglycemia have a defect in the two predominant phagocytic pathways of these cells. Given that phagocytosis is linked to activation of effector mechanisms for bacterial killing, it is likely that this defect is one factor contributing to the higher susceptibility of DM2 patients to pathogens like M. tuberculosis.

Indexed as

PhagocytosisAdultAnimalsChronic DiseaseDiabetes Mellitus, Type 2FemaleFlow CytometryFluorescenceHumansHyperglycemiaMaleMiddle AgedMonocytesPhenotypeReceptors, ComplementReceptors, IgGReceptors, ComplementReceptors, IgG

Identifiers

PMID24671137
PMCPMC3966862
OpenAlexW1964521000

What OpenQuestion holds

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LicenceCC BY
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.