Evidence map›Paper›PMID 37953267›Full record

ArticleCellular & molecular biology letters2023

Exosomal miR-155-5p drives widespread macrophage M1 polarization in hypervirulent Klebsiella pneumoniae-induced acute lung injury via the MSK1/p38-MAPK axis.

Yihan Xu, Chunying Zhang, Danni Cai, Rongping Zhu, Yingping Cao

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeting the non-coding RNA-PANoptosis axis: a novel frontier in disease diagnosis and therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. miRNA-146b TargetsAnimals : an open access journal from MDPI · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Lipoxin A4 AttenuatesJournal of inflammation research · 2026
    Article
  20. 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 at 1 institution in 1 country.

Yihan XuDepartment of Clinical Laboratory, Fujian Medical University Union Hospital, Fuzhou, 350001, People's Republic of China.
Chunying ZhangDepartment of Clinical Laboratory, Fujian Medical University Union Hospital, Fuzhou, 350001, People's Republic of China.
Danni CaiCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, 350001, People's Republic of China.
Rongping ZhuDepartment of Clinical Laboratory, Fujian Medical University Union Hospital, Fuzhou, 350001, People's Republic of China.
Yingping CaoDepartment of Clinical Laboratory, Fujian Medical University Union Hospital, Fuzhou, 350001, People's Republic of China. caoyingping@aliyun.com.ORCID http://orcid.org/0000-0002-0281-1515
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypervirulent Klebsiella pneumoniae (hvKp) infection-induced sepsis-associated acute lung injury (ALI) has emerged as a significant clinical challenge. Increasing evidence suggests that activated inflammatory macrophages contribute to tissue damage in sepsis. However, the underlying causes of widespread macrophage activation remain unclear.

methodsBALB/c mice were intravenously injected with inactivated hvKp (iHvKp) to observe lung tissue damage, inflammation, and M1 macrophage polarization. In vitro, activated RAW264.7 macrophage-derived exosomes (iHvKp-exo) were isolated and their role in ALI formation was investigated. RT-PCR was conducted to identify changes in exosomal miRNA. Bioinformatics analysis and dual-luciferase reporter assays were performed to validate MSK1 as a direct target of miR-155-5p. Further in vivo and in vitro experiments were conducted to explore the specific mechanisms involved.

resultsiHvKp successfully induced ALI in vivo and upregulated the expression of miR-155-5p. In vivo, injection of iHvKp-exo induced inflammatory tissue damage and macrophage M1 polarization. In vitro, iHvKp-exo was found to promote macrophage inflammatory response and M1 polarization through the activation of the p38-MAPK pathway. RT-PCR revealed exposure time-dependent increased levels of miR-155-5p in iHvKp-exo. Dual-luciferase reporter assays confirmed the functional role of miR-155-5p in mediating iHvKp-exo effects by targeting MSK1. Additionally, inhibition of miR-155-5p reduced M1 polarization of lung macrophages in vivo, resulting in decreased lung injury and inflammation induced by iHvKp-exo or iHvKp.

conclusionsThe aforementioned results indicate that exosomal miR-155-5p drives widespread macrophage inflammation and M1 polarization in hvKp-induced ALI through the MSK1/p38-MAPK Axis.

Indexed as

Acute Lung InjuryMicroRNAsSepsisAnimalsInflammationKlebsiella pneumoniaeLuciferasesMacrophage ActivationMacrophagesMiceLuciferasesMicroRNAsMirn155 microRNA, mouseAcute lung injuryExosomeHypervirulent Klebsiella pneumoniaeMacrophagemiR-155-5p

Identifiers

PMID37953267
PMCPMC10641976
OpenAlexW4388636803

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.