Lipopolysaccharide uptake is augmented in lipopolysaccharide-tolerant mouse macrophage-like cells via increased CD14 expression.

Saeka Nishihara, Takayuki Manabe, Mika Jouta, Kiyoshi Kawasaki

Abstract read

In one paragraph

Article in FEBS open bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing 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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Saeka NishiharaLaboratory of Biochemistry, Graduate School of Drug Discovery Sciences, Osaka Metropolitan University, Japan.

Takayuki ManabeDepartment of Nursing, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.

Mika JoutaFaculty of Pharmaceutical Sciences, Doshisha Women's University, Kyoto, Japan.

Kiyoshi KawasakiFaculty of Pharmaceutical Sciences, Doshisha Women's University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-7588-9436

Funding

Japan Society for the Promotion of Science 22K06607Promotion and Mutual Aid Corporation for Private Schools of Japan

6 · The paper itself

Abstract

Lipopolysaccharide (LPS) tolerance can be recognized as a modulation of innate immune responses rather than merely a hyporesponsiveness to LPS, with CD14 being crucial for both LPS uptake and LPS signaling. In this study, we observed that LPS-tolerant mouse macrophage-like cells, in which LPS-induced TNF-α and IFN-β production was suppressed, exhibited a dramatic increase in surface CD14 expression. Also, we found that LPS uptake was enhanced in LPS-tolerant mouse macrophage-like cells, but not when treated with an anti-CD14 antibody. While previous studies have reported increased CD14 expression and enhanced LPS uptake in LPS-tolerant cells, our findings reveal that overexpressed CD14 in LPS-tolerant mouse macrophage-like cells is responsible for the enhanced LPS uptake in these cells.

Indexed as

Lipopolysaccharide ReceptorsLipopolysaccharidesMacrophagesAnimalsImmunity, InnateInterferon-betaMiceSignal TransductionTumor Necrosis Factor-alphaCd14 protein, mouseInterferon-betaLipopolysaccharide ReceptorsLipopolysaccharidesTumor Necrosis Factor-alphaglycosylphosphatidylinositol‐anchored CD14innate immunityLPS hyporesponsiveness

Identifiers

PMID42037066

DOI10.1002/2211-5463.70261

PMCPMC13398632

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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.