Evidence map›Paper›PMID 34268870›Full record

ArticleMolecular nutrition & food research2021

Attenuation of Doxorubicin-Induced Small Intestinal Mucositis by Pectins is Dependent on Pectin's Methyl-Ester Number and Distribution.

Martin Beukema, Éva Jermendi, Taco Koster, Kohji Kitaguchi, Bart J de Haan, Marco Alexander van den Berg, Marijke M Faas, Henk A Schols, Paul de Vos

Open access · hybridAbstract read
In one paragraph

Article in Molecular nutrition & food research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

  1. Updated perspectives on the contribution of the microbiome to the pathogenesis of mucositis using the MASCC/ISOO framework.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024
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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

9 authors at 4 institutions in 2 countries.

Martin BeukemaDepartment of Pathology, Medical Biology and Immunoendocrinology, Division of Medical Biology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Éva JermendiLaboratory of Food Chemistry, Wageningen University, Bornse Weilanden 9, Wageningen, WG, 6708, The Netherlands.
Taco KosterDepartment of Pathology, Medical Biology and Immunoendocrinology, Division of Medical Biology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Kohji KitaguchiDepartment of Applied Life Science, Faculty of Applied Biological Sciences, Gifu University, 1-1 Yanagido, Gifu City, 501-1193, Japan.
Bart J de HaanDepartment of Pathology, Medical Biology and Immunoendocrinology, Division of Medical Biology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Marco Alexander van den BergDSM Biotechnology Center, Alexander Fleminglaan 1, Delft, AX, 2613, The Netherlands.
Marijke M FaasDepartment of Pathology, Medical Biology and Immunoendocrinology, Division of Medical Biology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Henk A ScholsLaboratory of Food Chemistry, Wageningen University, Bornse Weilanden 9, Wageningen, WG, 6708, The Netherlands.ORCID 0000-0002-5712-1554
Paul de VosDepartment of Pathology, Medical Biology and Immunoendocrinology, Division of Medical Biology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
University Medical Center Groningen · NLWageningen University & Research · NLDSM (Netherlands) · NLGifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

scopeIntestinal mucositis is a common side effect of the chemotherapeutic agent doxorubicin, which is characterized by severe Toll-like receptor (TLR) 2-mediated inflammation. The dietary fiber pectin is shown to prevent this intestinal inflammation through direct inhibition of TLR2 in a microbiota-independent manner. Recent in vitro studies show that inhibition of TLR2 is determined by the number and distribution of methyl-esters of pectins. Therefore, it is hypothesized that the degree of methyl-esterification (DM) and the degree of blockiness (DB) of pectins determine attenuating efficacy on doxorubicin-induced intestinal mucositis. METHODS AND

resultsFour structurally different pectins that differed in DM and DB are tested on inhibitory effects on murine TLR2 in vitro, and on doxorubicin-induced intestinal mucositis in mice. These data demonstrate that low DM pectins or intermediate DM pectins with high DB have the strongest inhibitory impact on murine TLR2-1 and the strongest attenuating effect on TLR2-induced apoptosis and peritonitis. Intermediate DM pectin with a low DB is, however, also effective in preventing the induction of doxorubicin-induced intestinal damage.

conclusionThese pectin structures with stronger TLR2-inhibiting properties may prevent the development of doxorubicin-induced intestinal damage in patients undergoing chemotherapeutic treatment with doxorubicin.

Indexed as

AnimalsAntibiotics, AntineoplasticAnti-Inflammatory Agents, Non-SteroidalApoptosisCell LineDose-Response Relationship, DrugDoxorubicinEsterificationFemaleIntestinal DiseasesIntestinal MucosaIntestine, SmallMiceMice, Inbred C57BLMucositisPectinsAntibiotics, AntineoplasticAnti-Inflammatory Agents, Non-SteroidalDoxorubicinPectinsTlr2 protein, mouseToll-Like Receptor 2chemotherapydegree of blockinessdegree of methyl-esterificationdoxorubicinmucositispectin

Identifiers

PMID34268870
PMCPMC8519125
OpenAlexW3182207591

What OpenQuestion holds

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LicenceCC BY
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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.