ArticleCellular and molecular life sciences : CMLS2024
Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
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.
Who cites it
26 citing papers in PubMed.
- Gut microbiota-immune-metabolic crosstalk in acute lung injury: integrating the gut-lung axis from mechanism to therapeutic targeting.Seminars in immunopathology · 2026Review
- Short-Chain Fatty Acids in Sepsis: Mechanisms of Action and Therapeutic Advances.Biomedicines · 2026Review
- Review
- SMURF2-Mediated Ubiquitination and Degradation of HOXA5 Augments Endoplasmic Reticulum Stress in Alveolar Epithelial Type II Cells Induced by LPS.Molecular biotechnology · 2026Article
- Synthesis and efficacy of tetraacetyl vitamin C ester: a novel alternative to traditional vitamin C and sodium acetate in aquafeeds.Journal of animal science and biotechnology · 2026Article
- The Regulatory Role of FABP4 in Microbiome-Brain-Gut Communication Under High-Fat-Diet Conditions.International journal of molecular sciences · 2026Review
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- Exploring the protective mechanisms and therapeutic potential of carnosic acid against acute respiratory distress syndrome through molecular docking, molecular dynamics and experimental verification.Experimental and therapeutic medicine · 2026Article
- Epigallocatechin Gallate Influences in Acute Respiratory Distress Syndrome by Regulating Gut Microbiota: Current Research Status and Therapeutic Prospects.Journal of inflammation research · 2026Review
- Neutrophil in sepsis: functional aberration and regulated cell death.Frontiers in immunology · 2026Review
- Short-Chain Fatty Acids: A Key Modulator of Sepsis-Associated Acute Respiratory Distress Syndrome.Journal of inflammation research · 2026Review
- Gut barrier-microbiota crosstalk in sepsis: from pathogenesis to potential therapies.Frontiers in immunology · 2026Review
- Comparative predictive value of nine inflammation-derived haematological indices for 28-day mortality in patients with sepsis: a multicentre retrospective cohort study.Frontiers in medicine · 2026Article
- Gut microbiota in acute lung injury/acute respiratory distress syndrome: mechanistic insights and therapeutic opportunities via the gut-lung axis.Frontiers in cellular and infection microbiology · 2026Review
- Gut microbiota dysbiosis in sepsis and sepsis-associated organ injury: mechanisms, gut-organ axes, and therapeutic strategies.Frontiers in microbiology · 2026Review
- Decoding the lncRNA-miRNA-mRNA network in sepsis-induced lung injury: from pathogenesis to extracellular vesicle-based therapy.Frontiers in immunology · 2026Review
- Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome.Journal of inflammation research · 2026Review
- Article
- Advances in Understanding the Impact of Human Gut Microbiota on Chemotherapy-Induced Neutropenia.Biomedicines · 2025Review
- Deep data-independent acquisition-based plasma proteomic profiling unveils distinct molecular features in dengue fever with neutropenia.Virologica Sinica · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
In patients with sepsis, neutrophil apoptosis tends to be inversely proportional to the severity of sepsis, but its mechanism is not yet clear. This study aimed to explore the mechanism of fatty acid binding protein 4 (FABP4) regulating neutrophil apoptosis through combined analysis of gut microbiota and short-chain fatty acids (SCFAs) metabolism. First, neutrophils from bronchoalveolar lavage fluid (BALF) of patients with sepsis-induced acute respiratory distress syndrome (ARDS) were purified and isolated RNA was applied for sequencing. Then, the cecal ligation and puncture (CLP) method was applied to induce the mouse sepsis model. After intervention with differential SCFAs sodium acetate, neutrophil apoptosis and FABP4 expression were further analyzed. Then, FABP4 inhibitor BMS309403 was used to treat neutrophils. We found CLP group had increased lung injury score, lung tissue wet/dry ratio, lung vascular permeability, and inflammatory factors IL-1β, TNF-α, IL-6, IFN-γ, and CCL3 levels in both bronchoalveolar lavage fluid and lung tissue. Additionally, FABP4 was lower in neutrophils of ARDS patients and mice. Meanwhile, CLP-induced dysbiosis of gut microbiota and changes in SCFAs levels were observed. Further verification showed that acetic acids reduced neutrophil apoptosis and FABP4 expression via FFAR2. Besides, FABP4 affected neutrophil apoptosis through endoplasmic reticulum (ER) stress, and neutrophil depletion alleviated the promotion of ARDS development by BMS309403. Moreover, FABP4 in neutrophils regulated the injury of RLE-6TN through inflammatory factors. In conclusion, FABP4 affected by gut microbiota-derived SCFAs delayed neutrophil apoptosis through ER stress, leading to increased inflammatory factors mediating lung epithelial cell damage.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.