Adipose‑derived mesenchymal stem cell‑derived HCAR1 regulates immune response in the attenuation of sepsis.
Wang H., Xuan P., Tian H., Hao X., Yang J., Xu X.
Animal Study with a reported sample of 6 on Chronic Inflammation, published in Mol Med Rep (2022) — summary generated from the PubMed abstract.
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
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
- Mol Med Rep (2022)
- Country
- Greece
- Reported sample size
- 6
- Source database
- PubMed
- PMID
- 35856408
- PMCID
- PMC9364135
- DOI
- 10.3892/mmr.2022.12795
- Citations
- 4
Abstract (original English)
Sepsis serves as a leading cause of admission to and death of patients in the intensive care unit (ICU) and is described as a systemic inflammatory response syndrome caused by abnormal host response to infection. Adipose‑derived mesenchymal stem cells (ADSCs) have exhibited reliable and promising clinical application potential in multiple disorders. However, the function and the mechanism of ADSCs in sepsis remain elusive. In the present study, the crucial inhibitory effect of ADSC‑derived hydroxy‑carboxylic acid receptor 1 (HCAR1) on sepsis was identified. Reverse transcription quantitative‑PCR determined that the mRNA expression of HCAR1 was reduced while the mRNA expression of Toll‑like receptor 4 (TLR4), major histocompatibility complex class II (MHC II), NOD‑like receptor family pyrin domain containing 3 (NLRP3), and the levels of interleukin‑1β (IL‑1β), tumor necrosis factor‑α (TNF‑α), interleukin‑10 (IL‑10), and interleukin‑18 (IL‑18) were enhanced in the peripheral blood of patients with sepsis. The expression of HCAR1 was negatively correlated with TLR4 (r=‑0.666), MHC II (r=‑0.587), and NLRP3 (r=‑0.621) expression and the expression of TLR4 was positively correlated with NLRP3 (r=0.641), IL‑1β (r=0.666), TNF‑α (r=0.606), and IL‑18 (r=0.624) levels in the samples. Receiver operating characteristic (ROC) curve analysis revealed that the area under the ROC curve (AUC) of
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.
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