---
title: "Adipose-derived MSC Exosomes Reduce LPS-induced Acute Lung Injury in Mice via the TGFBR2/Smad4–NLR"
id: "frontiers-in-immunology-18-adipose-derived-mesenchymal-stem-cell-exosomes-attenuate-lipopolysaccharide"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-18-adipose-derived-mesenchymal-stem-cell-exosomes-attenuate-lipopolysaccharide"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1739115"
published_at: "2026-09-14T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Adipose-derived MSC Exosomes Reduce LPS-induced Acute Lung Injury in Mice via the TGFBR2/Smad4–NLR
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-18-adipose-derived-mesenchymal-stem-cell-exosomes-attenuate-lipopolysaccharide
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1739115)
- **Published At:** 2026-09-14T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The study reports that **adipose-derived mesenchymal stem cell-exosomes** (ADSC-exosomes) attenuate **lipopolysaccharide (LPS)-induced acute lung injury (ALI)** in a mouse model, as stated in the article title published in Frontiers in Immunology. - The protective effect is attributed to modulation of the **TGFBR2/Smad4 axis**, indicating a regulatory interaction between exosome content and this signaling pathway. - Downstream of TGFBR2/Smad4, suppression of **NLRP3** inflammasome–related processes is implicated, specifically reducing **macrophage M1 polarization** and **pyroptosis**. - The model described is preclinical and uses mice challenged with LPS to induce lung injury; the intervention is ADSC-derived exosomes administered in that context. - The title indicates mechanistic connections (exosome → TGFBR2/Smad4 → reduced NLRP3 activity → decreased M1 polarization and pyroptosis) but the source text provided does not include experimental details, quantitative results, dosing, timing, or statistical outcomes. - Critical procedural and outcome information (number of animals, exosome isolation and characterization methods, routes and timing of administration, histology, inflammatory marker levels, and functional respiratory measures) were not reported in the supplied source content. - Translational implications are suggested by the mechanism-focused finding, but specific statements about safety, dose translation, or clinical recommendations are not provided in the source text. - Overall, the available information confirms a reported mechanism by which ADSC-derived exosomes mitigate LPS-induced ALI in mice through modulation of **TGFBR2/Smad4** and suppression of **NLRP3-mediated** macrophage-driven inflammation and cell death.
## Clinical Analysis & Structured Key Points
Frontiers | Adipose-derived mesenchymal stem cell-exosomes attenuate lipopolysaccharide-induced acute lung injury in mice by regulating the TGFBR2/Smad4 axis to suppress NLRP3-mediated macrophage M1 polarization and pyroptosis ORIGINAL RESEARCH article Front. Immunol. , 14 September 2026 Sec. Inflammation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1739115 Published in Frontiers in Immunology Inflammation 7 impact factor 11.3 citescore Editor & Reviewers Edited by B L Bruno L. Diaz Reviewed by J D Johnatas Dutra Silva S U Sadiq Umar Outline Figures and Tables Figure 1 View in article Figure 2 View in article Figure 3 View in article Figure 4 View in article Figure 5 View in article Figure 6 View in article Figure 7 View in article Table 1 Primer sequences of each gene. View in article ORIGINAL RESEARCH article Front. Immunol. , 14 September 2026 Sec. Inflammation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1739115 Adipose-derived mesenchymal stem cell-exosomes attenuate lipopolysaccharide-induced acute lung injury in mice by regulating the TGFBR2/Smad4 axis to suppress NLRP3-mediated macrophage M1 polarization and pyroptosis J L Jie Li 1,2 † * H K Huan Kang 2 † B W Baolong Wang 2 F Z Fangqiang Zou 2 W L Wei Liu 2 W G Weixin Guo 1 X L Xinliang Liao 3 * 1. Department of Geriatric Intensive Care Medicine, Guangdong Provincial Geriatrics Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China 2. Department of Intensive Care Medicine, Geriatric Center, National Regional Medical Center, Guangdong Provincial People’s Hospital Ganzhou Hospital, Ganzhou Municipal Hospital, Ganzhou, Jiangxi, China 3. Department of Geriatrics, Geriatric Center, National Regional Medical Center, Guangdong Provincial People’s Hospital Ganzhou Hospital, Ganzhou Municipal Hospital, Ganzhou, Jiangxi, China See more Article metrics View details Abstract Objective: This study investigated whether adipose-derived mesenchymal stem cells-exosomes (ADMSC-Exo) alleviate lipopolysaccharide (LPS)-induced acute lung injury (ALI) by regulating NLRP3 inflammasome-mediated macrophage M1 polarization and pyroptosis through the miR-19b-3p/TGFBR2/Smad4 signaling axis. Methods: An LPS-induced mouse model of ALI was established and treated with ADMSC-Exo or adenoviral TGFBR2 overexpression (Ad-TGFBR2). Lung histopathology, lung wet-to-dry (W/D) weight ratio, macrophage polarization, and pyroptosis were evaluated. In vitro , macrophages with TGFBR2 knockdown or overexpression were stimulated with LPS and treated with ADMSC-Exo. Lung epithelial cells were subsequently cultured with macrophage-conditioned medium. The expression of miR-19b-3p, TGFBR2, mothers against decapentaplegic homolog 4 (Smad4), and NOD-like receptor protein 3 (NLRP3), together with macrophage polarization, pyroptosis, and epithelial cell apoptosis, was assessed. Predicted molecular interactions were validated using bioinformatic analyses and the JASPAR database. Results: ADMSC-Exo alleviated LPS-induced lung injury by preserving alveolar architecture and reducing lung injury scores and the W/D ratio. They inhibited M1 macrophage polarization and pyroptosis both in vivo and in vitro , thereby decreasing apoptosis of lung epithelial cells. Mechanistically, ADMSC-Exo-delivered miR-19b-3p, which targeted TGFBR2 and inhibited TGFBR2/Smad4 signaling, resulting in transcriptional suppression of NLRP3 expression. Inhibition of miR-19b-3p or overexpression of Smad4/NLRP3 partially abolished the protective effects of ADMSC-Exo. Collectively, ADMSC-Exo attenuated LPS-induced ALI by suppressing NLRP3-mediated macrophage M1 polarization and pyroptosis through the miR-19b-3p/TGFBR2/Smad4 signaling axis. Conclusion: ADMSC-derived exosomes alleviate LPS-induced acute lung injury by delivering miR-19b-3p to inhibit the TGFBR2/Smad4 signaling pathway, thereby suppressing NLRP3-mediated macrophage M1 polarization and pyroptosis and reducing lung epithelial cell apoptosis. 1 Introduction Sepsis is a life-threatening syndrome characterized by organ dysfunction resulting from a dysregulated host response to infection ( 1 , 2 ). Among the organs affected, the lung is particularly susceptible during the early stage of sepsis ( 3 ), frequently progressing to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Increasing evidence indicates that dysregulated forms of programmed cell death, including autophagy, ferroptosis, and pyroptosis, contribute to the pathogenesis of lipopolysaccharide (LPS)-induced ALI, and therapeutic strategies targeting these pathways have shown protective effects in experimental models of LPS or cecal ligation and puncture-induced lung injury ( 4 ). Notably, macrophages play a central role in the initiation and progression of ALI/ARDS by orchestrating inflammatory responses ( 5 ). Excessive M1 macrophage polarization and pyroptosis have both been implicated in LPS-induced ALI ( 6 ), while inhibition of the C3a receptor attenuates lung injury by suppressing pyroptosis in pulmonary endothelial cells ( 7 ). Although macrophage polarization and pyroptosis are recognized as critical contributors to inflammatory tissue injury, the mechanistic interplay between these processes during LPS-induced ALI remains incompletely understood. Mesenchymal stem cells (MSCs) possess potent self-renewal capacity, immunomodulatory activity, and multilineage differentiation potential, making them attractive candidates for regenerative therapy ( 8 ). Among them, adipose-derived mesenchymal stem cells (ADMSCs) are particularly appealing because of their abundance, accessibility, and therapeutic efficacy in inflammatory diseases, including sepsis ( 9 ). Experimental studies have shown that ADMSCs attenuate LPS-induced ALI while improving gut microbiota dysbiosis in septic animals ( 10 ). More recently, increasing attention has shifted toward the therapeutic effects of exosomes released by MSCs, which reproduce many of the beneficial paracrine actions of their parental cells while avoiding several limitations associated with cell-based therapy. ADMSC-derived exosomes (ADMSC-Exo) have been shown to alleviate sepsis-induced inflammation by reducing inflammatory cytokine production and tissue injury ( 11 ). For example, Wang et al. demonstrated that ADMSC-Exo ameliorated sepsis-induced lung injury by suppressing macrophage-derived interleukin-27 (IL-27) production ( 12 ). In addition, ADSC-Exos inhibit NLRP3 inflammasome activation and pyroptosis while promoting macrophage polarization from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype, thereby alleviating ALI ( 13 ). Similarly, depletion of angiopoietin-like 4 attenuates LPS-induced ALI through inhibition of NF-κB activation, accompanied by reduced M1 macrophage polarization and NLRP3 inflammasome-mediated pyroptosis ( 14 ). Despite these observations, the molecular mechanisms by which ADMSC-Exo regulate NLRP3 inflammasome-dependent macrophage polarization and pyroptosis during LPS-induced ALI remain largely undefined. Transforming growth factor beta receptor II (TGFBR2) has recently emerged as an important regulator of inflammatory injury. TGFBR2 expression is markedly increased in patients with sepsis and in LPS-stimulated human bronchial epithelial BEAS-2B cells, whereas its silencing promotes cell viability and attenuates inflammatory responses ( 15 ). In addition, ADMSC-Exo carrying miR-671 alleviates myocardial infarction by targeting the TGFBR2/Smad2 signaling pathway ( 16 ), suggesting that exosomal microRNAs may regulate TGFBR2 signaling in inflammatory diseases. However, whether ADMSC-Exo protects against LPS-induced ALI through modulation of TGFBR2 and the underlying molecular mechanisms remain to be further elucidated. To identify potential upstream regulators of TGFBR2, microRNAs (miRNAs) enriched in mouse-derived exosomes were retrieved from the ExoCarta database, candidate miRNAs targeting TGFBR2 were predicted using multiple bioinformatic databases, and 27 differentially expressed miRNAs associated with sepsis were collected from published studies ( 17 ). Integration of these datasets using the Jvenn online platform identified miR-19b-3p as a shared candidate enriched in ADMSC-Exo, with predicted binding to TGFBR2. Previous studies have shown that miR-19b-3p is downregulated in patients with sepsis and that its overexpression alleviates LPS-induced inflammatory responses ( 18 ). However, whether ADMSC-Exo exert their protective effects against LPS-induced ALI by delivering miR-19b-3p to regulate TGFBR2 expression has not yet been investigated. Canonical transforming growth factor-β (TGF-β) signaling is initiated through activation of type I and type II serine/threonine kinase receptors (TβRI and TβRII). Following receptor activation, Smad2 and Smad3 are phosphorylated and subsequently form a transcriptional complex with mothers against decapentaplegic homolog 4 (Smad4) ( 19 ), which translocates into the nucleus to regulate target gene transcription ( 20 ). Consistent with its role in inflammatory signaling, Smad4 expression is increased in LPS-stimulated human pulmonary microvascular endothelial cells ( 21 ), whereas hydrogen treatment attenuates septic encephalopathy in mice by reducing Smad4 expression ( 22 ). Furthermore, TGFBR2 activates downstream TGF-β/Smad signaling ( 23 ), and upregulation of TGFBR2 has been shown to promote LPS-induced sepsis progression through activation of the TGFBR2/Smad pathway ( 24 ). As the common transcriptional mediator of this pathway, Smad4 directly regulates the transcription of multiple downstream genes ( 25 ). Bioinformatic analysis using the JASPAR database further predicted putative Smad4-binding sites within the NLRP3 promoter, suggesting a potential transcriptional link between TGFBR2/Smad signaling and NLRP3 inflammasome activation. Based on these findings, we hypothesized that ADMSC-Exo deliver miR-19b-3p to suppress TGFBR2 expression, thereby inhibiting Smad4-mediated transcriptional activation of NLRP3. This signaling cascade may suppress macrophage M1 polarization and pyroptosis, ultimately attenuating LPS-induced acute lung injury. Therefore, the present study aimed to elucidate the role of the miR-19b-3p/TGFBR2/Smad4/NLRP3 signaling axis in the protective effects of ADMSC-Exo and to provide mechanistic insights into exosome-based therapeutic strategies for sepsis-associated ALI. 2 Materials and methods 2.1 Ethics statement All animal procedures were approved by the Medical Ethics Committee of Guangdong Provincial People’s Hospital Ganzhou Hospital, Ganzhou Municipal Hospital (Approval no. SKJJ2024001A) and conducted in accordance with institutional guidelines for the care and use of laboratory animals. Every effort was made to minimize animal use and alleviate animal suffering throughout the study. 2.2 Bioinformatics analysis The ExoCarta database ( http://www.exocarta.org/ ) was queried to identify miRNAs enriched in mouse-derived exosomes, yielding 1, 455 candidate miRNAs ( Supplementary File 1 ). Candidate upstream miRNAs targeting TGFBR2 were predicted using the StarBase ( https://rnasysu.com/encori/ ), miRDB ( https://mirdb.org/ ), and miRWalk ( http://mirwalk.umm.uni-heidelberg.de/ ) databases ( Supplementary Files 2–4 ). In addition, 27 sepsis-associated differentially expressed miRNAs were collected from a previous study ( 17 ) ( Supplementary File 5 ). Candidate miRNAs were identified by intersecting these datasets using the Jvenn online website ( https://jvenn.toulouse.inra.fr/app/example.html ), which identified miR-19b-3p as a potential ADMSC-derived exosomal miRNA targeting TGFBR2 ( Supplementary File 6 ). 2.3 Culture and characterization of ADMSCs Mouse ADMSCs (CP-M138, Procell, Wuhan, Hubei, China) were cultured in ADMSC complete medium (CM-M138, Procell) at 37 °C in a humidified incubator containing 5% CO 2 . The immunophenotype of ADMSCs was characterized by flow cytometry. Cells were harvested by trypsinization, centrifuged at 800 × g for 6 min, washed with phosphate-buffered saline (PBS), and incubated with fluorescein isothiocyanate (FITC)-conjugated antibodies CD29-FITC (G0571, Selleck), CD34-FITC (G0121, Selleck), CD44-FITC (ab25064, Abcam), and CD45-FITC (ab210225, Abcam). Subsequent flow cytometric detection was performed using a FACSCalibur flow cytometer (Becton Dickinson, USA) equipped with FlowJo software (version vX 0.7) to identify the phenotypic characteristics of ADMSCs. The multilineage differentiation potential of ADMSCs was further evaluated as previously described ( 26 , 27 ). For osteogenic differentiation, 3 × 10 4 cells were seeded into six-well plates and cultured in osteogenic induction medium for 4 weeks, followed by fixation with 4% paraformaldehyde (PFA) for 20 min and staining with 1% Alizarin Red S solution (G1450, Solarbio). For adipogenic differentiation, 2 × 10 4 cells were cultured in adipogenic induction medium A for 3 days, followed by medium B for 1 day, with the induction cycle repeated three times. Cells were then fixed with 4% PFA for 30 min and stained with Oil Red O (G1262, Solarbio). For chondrogenic differentiation, 2.5 × 10 5 cells were cultivated as pellet cultures in chondrogenic induction medium. After 21 days, pellets were fixed with 4% PFA, embedded in paraffin, sectioned, and stained with Alcian blue (G1562, Solarbio). Stained samples were washed with PBS and observed under an Olympus microscope (Tokyo, Japan). 2.4 Isolation, characterization, and grouping of ADMSC-derived exosomes Exosomes were isolated from ADMSC-conditioned medium by differential ultracentrifugation as previously described ( 28 ). Briefly, ADMSCs at 80 – 90% confluence (passages 3 – 5) were washed three times with PBS and cultured for 48 h in Dulbecco’s Modified Eagle Medium/Ham’s F-12 supplemented with 10% exosome-depleted fetal bovine serum (Umibio, Shanghai, China). Conditioned medium was sequentially centrifuged at 300 × g for 20 min, 2, 000 × g for 30 min, and 12, 000 × g for 30 min at 4 °C to remove cells and debris. The supernatant was filtered through a 0.22-µm membrane filter (Millipore, Billerica, MA, USA) and ultracentrifuged at 100, 000 × g using a Beckman Coulter Optima L-80 XP ultracentrifuge to pellet exosomes. The exosome pellet was resuspended in 100 – 200 μL PBS solution and stored at -80 °C until further use ( 29 ). Exosome morphology was examined by transmission electron microscopy (TEM; Tecnai G2, FEI, USA), while particle size distribution and concentration were determined by nanoparticle tracking analysis (NTA; Malvern Panalytical, Worcestershire, UK). Western blot analysis was performed to detect the exosomal markers, including CD9 (1:1000, ab236630, Abcam), CD81 (1:1000, ab109201, Abcam), and Tsg101 (1:1000, ab133586, Abcam), together with the negative control marker Calnexin (1:1000, ab241154, Abcam). Culture supernatants from ADMSCs treated with GW4869 (10 μM), an inhibitor of exosome secretion, served as the negative control (GW) ( 30 ). Exosomal protein concentration was determined using a bicinchoninic acid (BCA) protein assay kit (P0010, Beyotime, Shanghai, China), and the protein-to-particle ratio was approximately 1 μg per 7.4 × 10 9 particles. For functional experiments, exosomes were divided into four groups: (1) GW group; (2) Exos group; (3) Exo-antag NC group: exosomes isolated from ADMSCs treated with 1 µM of the antagonist NC for 48 h; (4) Exo-miR antag group: exosomes isolated from ADMSCs treated with 1 µM of the miR-19b-3p antagonist for 48 h ( 31 ). For exosome preparation, ADMSCs were transfected with 1 μM antagonist NC or miR-19b-3p antagonist (GENECHEM Co., Ltd., Shanghai, China) for 48 h before exosome isolation. 2.5 Experimental animals Male C57BL/6 mice (8 weeks old, 18-22g) were purchased from Guangzhou Ruige Biotechnology Co., Ltd. (Guangzhou, China). Animals were housed under specific pathogen-free conditions with free access to food and water under a 12-h light/dark cycle at 22–24 °C and 45-55% humidity. 2.6 LPS-induced acute lung injury model Following one week of acclimatization, acute lung injury (ALI) was induced by intraperitoneal injection of lipopolysaccharide (LPS, 10 mg/kg) as previously described ( 29 ). For gene manipulation, mice received a tail vein injection of 20 μ adenoviral vectors (1 × 10 7 particles/μL) expressing Ad-NC, Ad-TGFBR2, Ad-sh-NC, or Ad-sh-TGFBR2 one week before LPS administration ( 32 ). One hour after LPS injection, mice were intravenously administered 100 μg ADMSC-derived exosomes (7.4 × 10 9 particles/μg in 100 μL PBS), Exos-antag NC, Exos-miR-19b-3p antag, or an equal volume of PBS ( 29 ). All adenoviral vectors were purchased from GENECHEM (Shanghai, China). Mice were randomly assigned to ten groups (n = 6 per group): (1) Control group; (2) LPS group; (3) LPS + PBS group: LPS-induced mice received an equal volume of PBS (100 μL) via tail vein injection, equivalent to that of ADMSC-Exo; (4) LPS + Exos group: LPS-induced mice received a tail vein injection of ADMSC-Exo; (5) LPS + Exos + Ad-NC group: LPS-induced mice were injected with the Ad-NC adenoviral vector via tail vein, followed by an ADMSC-Exo injection; (6) LPS + Exos + Ad-TGFBR2 group: LPS-induced mice underwent an tail vein injection of the adipose-derived transforming growth factor beta receptor II (Ad-TGFBR2) adenoviral vector, followed by ADMSC-Exo; (7) LPS + Exos-antag NC group: LPS-induced mice received Exos-antagonist NC via a tail vein injection; (8) LPS + Exos-miR antag group: LPS-induced mice received an Exos-miR-19b-3p antagonist injection via tail vein; (9) LPS + Exos-miR antag + Ad-sh-NC group: LPS-induced mice were injected with Exos-miR-19b-3p antagonist after a tail vein injection of Ad-sh-NC; (10) LPS + Exos-miR antag + Ad-sh-TGFBR2 group: LPS-induced mice were subjected to a tail intravenous injection of Ad-sh-TGFBR2, before an Exos-miR-19b-3p antagonist injection. Twenty-four hours after LPS administration, mice were euthanized under isoflurane anesthesia ( 33 ). Briefly, mice were placed in an induction chamber with 5% isoflurane. An appropriate anesthetic plane was achieved within 1 min, confirmed by complete loss of consciousness and disappearance of the righting and pedal reflexes. Mice were immediately removed from the chamber and maintained under anesthesia with 2%–3% isoflurane via a face mask, followed by rapid cervical dislocation to confirm euthanasia ( 34 ). Lung tissues were immediately harvested afterwards. The left lung was divided for histological examination and tissue homogenization, whereas the right lung was used for determination of the wet-to-dry (W/D) weight ratio. Randomization and investigator blinding were implemented throughout the animal study. Mice were allocated to experimental groups using a random number table. Animal allocation, experimental procedures, outcome assessment, and statistical analyses were conducted by independent investigators blinded to group assignments. Mice that died before completion of the experimental protocol were predefined as exclusion criteria; however, no animals died during the study, and all enrolled mice were included in the final analyses. 2.7 Hematoxylin and eosin staining Lung tissues were fixed in 4% paraformaldehyde, dehydrated through graded ethanol, cleared with xylene, embedded in paraffin, sectioned into 5-μm slices, and stained with hematoxylin and eosin (C0105S, Beyotime). Histopathological changes were examined under a light microscope (Olympus, Tokyo, Japan). Lung injury was evaluated using the blinded scoring system recommended by the American Thoracic Society ( 35 ). Briefly, alveolar wall thickening, pulmonary edema, and inflammatory cell infiltration/congestion were each scored on a scale of 0-3 (0 = absent, 1 = mild, 2 = moderate, and 3 = severe), yielding a maximu
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