Evidence map›Paper›PMID 40794263›Full record

ArticleGenes & genomics2025

Regulation of intracellular proliferation of Salmonella typhimurium by CD63.

Kwan Sik Park, In Sook Jeon, Jin Tae Hong, Bumhee Yang, Joong-Kook Choi

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Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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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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

2 citing papers in PubMed.

  1. Article
  2. Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025
    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

5 authors.

Kwan Sik Park *Division of Biochemistry, College of Medicine, Chungbuk National University, Cheongju, Chungbuk Province, Republic of Korea.
In Sook Jeon *Division of Biochemistry, College of Medicine, Chungbuk National University, Cheongju, Chungbuk Province, Republic of Korea.
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, 194-31, Osongsaengmyeong 1-ro, Osong-eup, Cheongju, Chungbuk Province, 28160, Republic of Korea.
Bumhee YangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Chungbuk National University Hospital, Cheongju, Chungbuk Province, Republic of Korea. ybhworld0415@gmail.com.
Joong-Kook ChoiDivision of Biochemistry, College of Medicine, Chungbuk National University, Cheongju, Chungbuk Province, Republic of Korea. jkchoi@chungbuk.ac.kr.ORCID http://orcid.org/0000-0003-0455-971X

Funding

National Research Foundation of Korea 2021R1I1A1A01046728National Research Foundation of Korea 2021R1I1A3058091Regional Innovation Strategy (RIS) 2021RIS-001
6 · The paper itself

Abstract

backgroundAutophagy is an intracellular degradation process involving the lysosomal breakdown of unnecessary or abnormal cellular components. Targets of autophagy include pathogens, altered organelles, and protein aggregates, which are sequestered within double-membrane-limited vesicles known as autophagosomes. A variety of lysosomal membrane proteins play essential roles in numerous cellular processes, including lysosomal acidification, metabolite transport, and interaction with other membrane systems. Cluster of differentiation 63 (CD63), a member of the transmembrane 4 superfamily, is present on the cell surface and in intracellular membrane compartments, such as endosomal and lysosomal membranes. This protein is also associated with several diseases, including Hermansky-Pudlak syndrome and immunoglobulin E-mediated allergies. However, its role in the autophagy pathway and intracellular bacterial proliferation remains poorly understood.

objectiveThis study aimed to investigate changes in CD63 expression in response to Salmonella infection and to analyze the effects of these changes on Salmonella proliferation.

methodsChanges in CD63 expression were examined following Salmonella infection using cellular models. Expression regulation was assessed for dependence on nuclear factor kappa B signaling. Colocalization of CD63 was evaluated with green fluorescent protein-tagged Salmonella and the lysosomal marker LysoTracker. Intracellular Salmonella titers were measured and correlated with CD63 expression levels to determine impacts on bacterial survival.

resultsCD63 expression increased in response to Salmonella infection in a nuclear factor kappa B-dependent manner. CD63 colocalized with green fluorescent protein-tagged Salmonella and the lysosomal marker LysoTracker. The titer of intracellular Salmonella was inversely correlated with CD63 expression, suggesting that higher CD63 levels reduce bacterial survival.

conclusionCD63 contributes to the regulation of intracellular Salmonella survival through the autophagy pathway, specifically xenophagy (autophagy targeting pathogens). This is the first report documenting the inhibition of Salmonella proliferation via induction of CD63 expression and Xenophagy.

Indexed as

Salmonella InfectionsSalmonella typhimuriumTetraspanin 30AutophagyHumansLysosomesNF-kappa BCD63 protein, humanNF-kappa BTetraspanin 30CD63Intracellular proliferationLysosomal proteinsSalmonellaXenophagy

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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.