Evidence map›Paper›PMID 32881912›Full record

Trial reportPloS one2020

Feasibility of quantifying change in immune white cells in abdominal adipose tissue in response to an immune modulator in clinical obesity.

Fred R Sattler, Melissa Mert, Ishwarya Sankaranarayanan, Wendy J Mack, Lauriane Galle-Treger, Evelyn Gonzalez, Lilit Baronikian, Kyuwan Lee, Pedram Shafiei Jahani, Howard N Hodis and 2 more

Open access · goldAbstract readClinical Trial, Phase IIIRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  2. Near-roadway air pollution, immune cells and adipokines among obese young adults.Environmental health : a global access science source · 2022
    Article
  3. Review
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

12 authors at 1 institution in 1 country.

Fred R SattlerDepartment of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.ORCID 0000-0002-1986-6803
Melissa MertDepartment of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Ishwarya SankaranarayananDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Wendy J MackDepartment of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Lauriane Galle-TregerDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Evelyn GonzalezDepartment of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Lilit BaronikianDepartment of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Kyuwan LeeOstrow School of Dentistry, Division of Physical Therapy and Biokinesiology, University of Southern California, Los Angeles, California, United States of America.
Pedram Shafiei JahaniDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Howard N HodisDepartment of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
Christina Dieli-ConwrightOstrow School of Dentistry, Division of Physical Therapy and Biokinesiology, University of Southern California, Los Angeles, California, United States of America.
Omid AkbariDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, United States of America.
University of Southern California · US

Funding

Southern California Clinical and Translational Science InstituteUL1TR001855 · NCATS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Thomas A Buchanan, Michele D. Kipke · 2016 to 2026
$81.3M
Induction of cells and pathways that promote respiratory tolerance in allergic asthmaR01HL144790 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2019 to 2022
$2.6M
NCATS NIH HHS UL1 TR001855NHLBI NIH HHS R01 HL144790
6 · The paper itself

Abstract

backgroundObesity is often associated with inflammation in adipose tissue (AT) with release of mediators of atherogenesis. We postulated that it would be feasible to collect sufficient abdominal AT to quantify changes in a broad array of adaptive and innate mononuclear white cells in obese non-diabetic adults in response to a dipeptidyl protease inhibitor (DPP4i), known to inhibit activation of immune white cells.

methodsAdults 18-55 years-of-age were screened for abdominal obesity and insulin resistance or impaired glucose tolerance but without known inflammatory conditions. Twenty-one eligible participants consented for study and were randomized 3:1 to receive sitagliptin (DPP4i) at 100mg or matching placebo daily for 28 days. Abdominal AT collected by percutaneous biopsy and peripheral blood mononuclear cell fractions were evaluated before and after treatment; plasma was stored for batch testing.

resultsHighly sensitive C-reactive protein, a global marker of inflammation, was not elevated in the study population. Innate lymphoid cells (ILC) type 3 (ILC-3) in abdominal AT decreased with active treatment compared with placebo (p = 0.04). Other immune white cells in AT and peripheral blood mononuclear cell (PBMC) fractions did not change with treatment compared to placebo (p>0.05); although ILC-2 declined in PBMCs (p = 0.007) in the sitagliptin treatment group. Two circulating biomarkers of atherogenesis, interferon-inducible protein-10 (IP-10) and sCD40L declined in plasma (p = 0.02 and p = 0.07, respectively) in the active treatment group, providing indirect validation of a net reduction in inflammation.

conclusionsIn this pilot study, two cell types of the innate lymphoid system, ILC-3 in AT and ILC-2 PBMCs declined during treatment and as did circulating biomarkers of atherogenesis. Changes in other immune cells were not demonstrable. The study showed that sufficient abdominal AT could be obtained to quantify white cells of both innate and adaptive immunity and to demonstrate changes during therapy with an immune inhibitor.

trial registrationClinicalTrials.gov identifier (NCT number): NCT02576.

Indexed as

Abdominal FatImmunity, InnateLeukocytes, MononuclearObesityAdultBiomarkersFeasibility StudiesFemaleFlow CytometryHumansLymphocytesMaleMiddle AgedPilot ProjectsSitagliptin PhosphateTreatment OutcomeBiomarkersSitagliptin Phosphate

Identifiers

PMID32881912
PMCPMC7470412
OpenAlexW3083566607

What OpenQuestion holds

Textmetadata
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.