Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Therapeutic potential of ADSC-derived exosomes in acute lung injury by regulating macrophage polarization through IRF7/NLRP3 signaling.

Ren J., Lei G., Dong A., Cao S., Han X., Li H.

Animal Study on Chronic Inflammation, Immune Modulation, published in Int Immunopharmacol (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Int Immunopharmacol (2025)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
40252464
DOI
10.1016/j.intimp.2025.114658
Citations
1

Abstract (original English)

Alveolar macrophages (AMs) play a critical role in regulating pulmonary immunity and inflammation. Acute lung injury (ALI), frequently initiated by sepsis-induced systemic inflammation and cytokine storms, leads to heightened lung permeability and respiratory failure. Adipose-derived stem cell exosomes (ADSC-Exos) have shown promise as therapeutic agents due to their immunomodulatory properties. This study assesses the effectiveness of ADSC-Exos in mitigating ALI by modulating macrophage (mø) polarization and suppressing pyroptosis. In vivo, an LPS-induced ALI mouse model demonstrated that ADSC-Exos attenuated lung tissue inflammation and damage, as verified by histological staining, ELISA, and immunofluorescence. In vitro, LPS-stimulated MH-S cells treated with ADSC-Exos showed a decrease in M1 (iNOS, CD86) and an increase in M2 (CD206, Arg-1) markers, as evidenced by Western blotting (WB) and flow cytometry. Mechanistically, RNA sequencing pinpointed IRF7 as a key upstream regulator of pyroptosis. ADSC-Exos inhibited the NLRP3 inflammasome and pyroptosis, fostering a shift from pro-inflammatory M1 to anti-inflammatory M2 mø phenotypes. Overexpression of IRF7 negated these effects, undermining the protective role of ADSC-Exos. Notably, inhibition of exosome secretion with GW4869 nullified these immunomodulatory effects, underscoring the vital role of ADSC-Exos. This study unde

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsExosomesNLR Family, Pyrin Domain-Containing 3 ProteinAcute Lung InjuryMiceSignal TransductionPyroptosisMice, Inbred C57BLMaleHumans

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