Evidence map›Paper›PMID 38189743›Full record

ArticleImmunoHorizons2024

LNCGM1082 in Gut Epithelial Cells Promotes Expulsion of Infected Epithelial Cells and Release of IL-18.

Ya Wang, Yunhuan Gao, Xiaomin Su, Yang Hao, Yuan Zhang, Rongcun Yang

Open access · goldAbstract read
In one paragraph

Article in ImmunoHorizons, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 100% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 2 institutions in 1 country.

Ya WangTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Yunhuan GaoTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Xiaomin SuTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Yang HaoTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Yuan ZhangTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Rongcun YangTranslational Medicine Institute, Tianjin Union Medical Center of Nankai University, Tianjin, China; Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China; and State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Tianjin Medical University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammasome NLRC4 (NLR family CARD domain containing 4) can protect mucosal barriers such as intestine from invading bacterial pathogens. However, it was incompletely clear how NLRC4 was activated in intestinal epithelial cells. In this study, we demonstrated that LNCGM1082 could mediate the activation of NLRC4 via binding NLRC4 with protein kinase C (PKC)δ. LNCGM1082 knockout (KO) mice had reduced resistance against Salmonella Typhimurium infection, as well as impaired expulsion of infected gut epithelial cells and release of IL-18 upon exposure to S. Typhimurium. Similar to NLRC4 KO and PKCδ knockdown gut organoids, there also was impaired expulsion of gut epithelial cells and release of IL-18 in LNCGM1082 KO gut organoids. Furthermore, there also was reduced activation of caspase-1 and caspase-8 in these LNCGM1082 KO, NLRC4 KO, and PKCδ knockdown gut organoids upon exposure to S. Typhimurium. Our results show that LNCGM1082 in the ICEs plays a critical role in mediating activation of NLRC4 through binding NLRC4 and PKCδ and promoting expulsion of infected epithelial cells and release of IL-18 upon exposure to bacteria such as S. Typhimurium.

Indexed as

Epithelial CellsInterleukin-18AnimalsInflammasomesMiceMice, KnockoutInflammasomesInterleukin-18

Identifiers

PMID38189743
PMCPMC10835649
OpenAlexW4390671346

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.