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Aqueous Artemisia argyi extract mitigates acute lung injury in association with coordinated alterations in gut microbiota, metabolic homeostasis, and pulmonary inflammatory gene expression

ABSTRACT: his study investigated the metabolic alterations in colonic contents associated with aqueous extract of Artemisia argyi (AEAA) intervention in a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. Male C57BL/6 mice were randomly divided into control, LPS, and AEAA treatment groups with low-, medium-, and high-dose administration.

AEAA was administered by oral gavage for 28 consecutive days. On day 29, ALI was induced by intratracheal instillation of LPS (5 mg/kg) in the LPS and treatment groups, while control mice received sterile saline. Colonic content samples were collected 8 hours after LPS administration.

Untargeted metabolomics analysis was performed using liquid chromatography¨Cmass spectrometry (LC-MS). Quality control (QC) samples were included to ensure analytical stability. The metabolomic profiles of colonic contents were analyzed to explore gut metabolic alterations and potential mechanisms underlying the protective effects of AEAA in acute lung injury.

This dataset provides raw LC-MS data of colonic content metabolomics and can be used to investigate gut-related metabolic pathways involved in inflammation and natural product intervention.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14155 | MetaboLights | 2026-03-27

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14155_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14155_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_REQ20260325218126_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_REQ20260325218126_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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Project description:Background: Artemisia argyi is a traditional medicinal herb with established anti-inflammatory and immunomodulatory properties. Its aqueous extract (AEAA), enriched in water-soluble bioactive constituents, exhibits favorable safety and bioavailability; however, its potential protective effects against acute lung injury (ALI) and its associations with systemic immunometabolic regulation remain incompletely understood. Methods: An LPS-induced ALI mouse model was established following 28 days of AEAA pretreatment. Lung histopathology, pulmonary edema, and inflammatory cytokines were evaluated. Integrated multi-omics analyses—including gut microbiota profiling, untargeted metabolomics of colonic contents and serum, and lung transcriptomics—were performed to characterize treatment-associated microbial, metabolic, and transcriptional alterations. Results: AEAA pretreatment dose-dependently alleviated lung injury, reduced pulmonary edema, and suppressed pro-inflammatory cytokines while restoring anti-inflammatory IL-10 levels. AEAA treatment was associated with partial reversal of LPS-induced gut dysbiosis, characterized by reduced abundance of inflammation-associated taxa and enrichment of beneficial genera, particularly Akkermansia and Lactobacillus. Metabolomic analyses revealed treatment-associated normalization of intestinal and systemic metabolic disturbances, including increased homeostasis-related metabolites and reduced inflammation-associated metabolites. Lung transcriptomic profiling suggested attenuation of LPS-associated transcriptional signatures related to NF-κB, MAPK, Toll-like receptor, and PI3K–AKT signaling pathways. Cross-omics integration further revealed coordinated associations among microbial shifts, metabolic remodeling, and pulmonary inflammatory gene expression. Conclusion: These findings suggest that aqueous Artemisia argyi extract is associated with mitigation of LPS-induced acute lung injury, accompanied by coordinated alterations in gut microbiota composition, host metabolic profiles, and pulmonary inflammatory gene expression. Although causal relationships were not established, this integrated multi-omics analysis provides a systems-level, hypothesis-generating framework supporting the potential of AEAA as a multi-target botanical candidate for ALI.

Project description:Acute lung injury (ALI), a major cause of acute respiratory failure with high morbidity and mortality, isare characterized by significant pulmonary inflammation and both alveolar and vascular barriers dysfunction. In Pprior studies have highlighted the role of nonmuscle myosin light chain kinase (nmMLCK) as an essential element of inflammatory response with MYLK polymorphisms associated withwhich alters ALI susceptibility. In the present study we sought to further define nmMLCK in acute inflammatory syndromes and examined We examined nmMLCK as a molecular target involved in increase of lung epithelial and endothelial barrier permeability. We utilized in two muirine models of inflammatory lung injury: intratracheal administration of endotoxin/lipopolysaccharide (LPS, 2.5 mg/kg) and VILI (ventilator-induced lung injury, tidal volume 40ml/kg). Two complementary strategies were used to reduce nmMLCK activity or expression. We found that membrane permeant oligopeptide, PIK, inhibited MLC kinase activity in vitro in aand displayed dose-dependent mannerinhibition of MLC kinase activity.. Intravenous delivery of PIK significantly attenuated LPS-induced lung inflammation reflected by decreasing accumulation of bronchoalveolar lavage (BAL) albumin (~ 50% reduction) as well as reduction in BAL cells, tissue MPO activity and tissue albumin in lung homogenates. A second regulatory approach explored targeting murine nmMLCK by administration of siRNA (5mg/kg) 3 days prior to LPS challenge. siRNA decreased of nmMLCK expression in lungs (~ 70% reduction) and resulted in significant attenuation LPS-induced lung inflammation (~ 40% reduction) as reflected by decreased BAL protein level and BAL cells. For targeting pulmonary vessels nmMLCK we used ACE antibody-conjugated liposomes with nmMLCK siRNA in murine ventilator-induced lung injury (VILI) model. Protein silencing of nmMLCK was evident by immunohistochemical analysis with a decrease in relative intensity of fluorescence in lung vessels compared with control animals. Furthermore, the inhibition of nmMLCK expression by siRNA in vessels significantly attenuated VILI lung injury as reflected by decreased BAL protein level (40% reduction). Finally, MLCK knockout mice were significantly protected (reduced BAL protein and albumin) when exposed to a model of severe VILI (4h, 40ml/kg tidal volume). Conclusion: the MLCK gene KO and chemical biology results indicate that the targeting of nmMLCK in vivo attenuate the severity of LPS-induced or VILI acute lung injury. We used microarrays to detail the global programme of gene expression induced by VILI in Wild type and nmMLCK-/- mouse. Experiment Overall Design: four group (n=3) of animals were treated by SB (Spontaneouse breathing) or VILI (4 hours, 30 ml/kg tidal volume) in Wild type or nmMLCK-/- animals;

Project description:Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an inflammatory process of the lungs characterized by increased permeability of the alveolar-capillary membrane with subsequent interstitial/alveolar edema and diffuse alveolar damage. ALI/ARDS can be the results of either direct or indirect lung injury, with pneumonia being the most common direct pulmonary insult and sepsis the most common extra-pulmonary cause. In this study, we employed the murine lipopolysaccharide (LPS)-induced direct and indirect lung injury model to explore the pathogenic mechanisms of pulmonary and extra-pulmonary ARDS, using an unbiased, discovery and quantitative proteomic approach. A total of 1,017 proteins were both identified and quantified in bronchoalveolar lavage fluid (BALF) from control, intratracheal LPS (I.T. LPS, 0.1 mg/kg) and intraperitoneal LPS (I.P. LPS, 5 mg/kg) treated mice. The two LPS groups shared 13 up-regulated and 22 down-regulated proteins compared to the control group. Among them, molecules related to bronchial and type II alveolar epithelial cell functions including cell adhesion molecule 1 and surfactant protein B were reduced, whereas lactotransferrin and resistin like alpha involved in lung innate immunity were upregulated in both LPS groups. Proteomic profiling also identified significant differences in BALF proteins between I.T. and I.P. LPS groups. Ingenuity pathway analysis revealed that acute-phase response signaling was activated by both I.T. and I.P. LPS, however, the magnitude of activation is much greater in I.T. LPS group compared to I.P. LPS group. Intriguingly, two canonical signaling pathways, liver X receptor/retinoid X receptor activation and the production of nitric oxide and reactive oxygen species in macrophages, were activated by I.T. LPS but suppressed by I.P. LPS. In addition, CXCL15 (also known as lungkine) was also up-regulated by I.T LPS but down-regulated by I.P. LPS. In conclusion, our quantitative discovery-based proteomic approach identified commonalities as well as significant differences in BALF protein expression profiles in LPS-induced direct and indirect lung injury, and importantly, LPS-induced indirect lung injury results in suppression of select components of lung innate immunity, which could contribute to the so-called “immunoparalysis” in sepsis patients.

Project description:Acute respiratory distress syndrome (ARDS) is a catastrophic form of acute lung injury (ALI). The necessity for mechanical ventilation (MV) renders patients at risk for ventilator induced lung injury (VILI). Exposure to repetitive cyclic stretch (CS) and/or over-inflation exacerbates injury. Reducing tidal volume (VT) is the only therapeutic strategy shown to mitigate morbidity and mortality. Cyclic stretch has been shown to differentially regulate gene expression in part through the activation of mammalian mitogen-activated protein kinase (MAPK). Although these studies have shown both molecular and cellular alterations, no unifying hypothesis to explain MV-induced lung injury has emerged. In the current study, we hypothesized that coordinated expression of cyclic stretch (CS)-responsive genes relies on the presence of common CS-sensitive regulatory elements. To identify CS-responsive genes, we undertook a comparative examination of the gene expression profile of human bronchial epithelial airway (Beas-2B) cells in response to various injurious stimuli involved in the pathogenesis of acute lung injury (ALI)/Ventilator induced lung injury (VILI): cyclic stretch, tumor necrosis factor alpha (TNF-a), and lipopolysaccharide (LPS). Experiment Overall Design: Human Bronchial Epithelial Cells (Beas-B2) cells grown on silicon elastic plates coated with Type I collagen (Flexercell International, McKeesport, PA) were exposed to six regiments for 4 h: 1) control (static, [control]); 2) mechanical stretch (25 PKa, 30 cycles per min, [stretch]); 3) LPS (1 mcg/ml [LPS]); 4) TNF-Î± (20 ng/ml; [TNF]); 5) mechanical stretch plus LPS [LPS+S], and 6) mechanical stretch plus TNF-Î± [TNF+S]. Total RNA (duplicate experiments) was extracted using TRIZOL reagent (as per manufactures specifications) and purified using Qiagen mRNA purification Kit (as per manufacturers specifications). mRNA was hybridized to Affymetrix Human U133plus2.0 chips. Probe based analysis, background reduction, and quantile data normalization was performed in MeV 4.0 of TM4 using Robust Multi-array Average (RMA).

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Aqueous Artemisia argyi extract mitigates acute lung injury in association with coordinated alterations in gut microbiota, metabolic homeostasis, and pulmonary inflammatory gene expression

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