Evidence map›Paper›PMID 16091914›Full record

ArticleInternational journal of colorectal disease2006

Inherent potential for production of tumor necrosis factor-alpha by human intestinal macrophages.

Kazue Nakata, Hiroyuki Inagawa, Takashi Nishizawa, Teruko Honda, Chie Kohchi, Yasuhito Tonomoto, Hiroshi Yoshimura, Naofumi Nagasue, Shynji Natori, Hiroshi Terada and 1 more

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Article in International journal of colorectal disease, 2006. 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
0.9field-weighted citation impact, top 25% 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, 11 citations in OpenAlex.

  1. Functional macrophages and gastrointestinal disorders.World journal of gastroenterology · 2018
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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

11 authors at 7 institutions in 1 country.

Kazue NakataInstitute for Health Sciences, Tokushima Bunri University, Yamashiro-cho, Tokushima, 770-8514, Japan.
Hiroyuki Inagawa
Takashi Nishizawa
Teruko Honda
Chie Kohchi
Yasuhito Tonomoto
Hiroshi Yoshimura
Naofumi Nagasue
Shynji Natori
Hiroshi Terada
Gen-Ichiro Soma
Tokyo University of Science · JPShimane University · JPTokushima Bunri University · JPKumamoto University · JPNational Fisheries University · JPRIKEN · JPUniversity of Shimane · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsTumor necrosis factor (TNF) production by the macrophages in intestines appears to play a critical role in the pathogenesis of Crohn's disease (CD). However, it is reported that resident intestinal macrophages (both colonic and small-bowel) do not produce TNF after lipopolysaccharide (LPS) stimulation. It has not yet been proven whether or not intestinal macrophages have an inherent potential to produce TNF. The purpose of this study is to answer this question. MATERIALS AND

methodsColonic macrophages were isolated from lamina propria of human large intestine and stimulated with a variety of substances: LPS, a lipid A derivative (ONO-4007), killed Streptococcus bacterial body (OK-432), phorbol 12-myristate 13-acetate, and lectins (pokeweed mitogen and Sarcophaga lectin).

resultsColonic macrophages were phenotypically negative for CD14 and positive for CD68 and produced very little TNF in response to LPS, as reported previously. Of the substances tested, only Sarcophaga lectin, which is a defense protein of fleshflies (Sarcophaga peregrina), induced TNF production by the intestinal macrophages. In addition, when the colonic macrophages were cultured on immunoglobulin-A-coated dishes, their characteristic response to LPS was altered, and they produced TNF at a level 6.6 times higher than when on collagen-coated dishes.

conclusionColonic macrophages have an inherent ability to produce TNF. Activation of colonic macrophages by unknown substances may contribute to the induction of TNF production, which causes the intestinal inflammation of CD.

Indexed as

Macrophage ActivationAntigens, CDAntigens, Differentiation, MyelomonocyticAntineoplastic AgentsCarcinogensCD68 MoleculeCells, CulturedCollagenColonCulture TechniquesHumansImmunoglobulin AInsect ProteinsLectins, C-TypeLipopolysaccharidesMacrophages20kDa lectin protein, SarcophagaAntigens, CDAntigens, Differentiation, MyelomonocyticAntineoplastic AgentsCarcinogensCD68 antigen, humanCD68 MoleculeCollagenImmunoglobulin AInsect ProteinsLectins, C-Typelipopolysaccharide ALipopolysaccharidesMitogensPicibanilPokeweed MitogensTetradecanoylphorbol AcetateTumor Necrosis Factor-alpha

Identifiers

PMID16091914
OpenAlexW1968833886

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.