Evidence map›Paper›PMID 39187364›Full record

ArticleIn vivo (Athens, Greece)

Lipopolysaccharide Derived from

Hiroyuki Inagawa, Takashi Nishizawa, Chie Kohchi, Gen-Ichiro Soma

Abstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

4 authors.

Hiroyuki InagawaControl of Innate Immunity, Collaborative Innovation Partnership, Kagawa, Japan.
Takashi NishizawaMacrophi Inc., Kagawa, Japan.
Chie KohchiControl of Innate Immunity, Collaborative Innovation Partnership, Kagawa, Japan.
Gen-Ichiro SomaControl of Innate Immunity, Collaborative Innovation Partnership, Kagawa, Japan; gensoma@shizenmeneki.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimBecause the skin is exposed to the external environment, it is important that wound healing processes proceed and terminate rapidly to minimize the risk of infection. A previous case report described the promotion of wound healing by transdermal administration of lipopolysaccharide derived from Pantoea agglomerans (LPSp). However, whether the wound healing-promoting effect of LPSp was due to direct activity on skin cells or indirect effects involving macrophages remained unclear. Therefore, this study investigated the wound healing-promoting effect of LPSp, particularly the promotion of keratinocyte migration. MATERIALS AND

methodsThe migration of HaCaT human keratinocytes over time with and without LPSp was assayed using a cell migration assay kit. Migration was also analyzed using HaCaT cells treated with LPSp and an antibody against Toll-like receptor (TLR) 4, a receptor for LPS.

resultsAddition of LPSp significantly enhanced cell migration compared to no LPSp addition. Migration was inhibited by the addition of anti-TLR4 antibody.

conclusionLPSp acts directly on epidermal cells to promote migration and may be one mechanism by which LPSp promotes wound healing.

Indexed as

Cell MovementKeratinocytesLipopolysaccharidesPantoeaWound HealingCell LineHumansToll-Like Receptor 4LipopolysaccharidesToll-Like Receptor 4keratinocytelipopolysaccharidemigrationPantoea agglomeransscratch assaywound healing

Identifiers

PMID39187364
PMCPMC11363747

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.