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Combined analysis of cecal microbiota and metabolomics reveals the intervention mechanism of Dayuan Yin in acute lung injury

ABSTRACT:

The ancient Chinese medicinal formula, Dayuan Yin (DYY), has a long history of use in treating respiratory ailments and shown to be effective in treating acute infectious diseases. This study aims to explore how DYY may impact intestinal flora and metabolites induced by acute lung injury (ALI). ALI rats were induced with lipopolysaccharide (LPS) to serve as models for assessing the anti-ALI efficacy of DYY through multiple lung injury indices. Changes in intestinal microflora were assessed via 16SrRNA gene sequencing, while cecum contents were analyzed using non-targeted metabonomics. Differential metabolites were identified through data analysis, and correlations between metabolites, microbiota and in flammatory markers were examined using Pearson correlation analysis. DYY demonstrated a significant improvement in LPS-induced lung injury and altered the composition of intestinal microorganisms, especially reduced the potential harmful bacteria and enriched the beneficial bacteria. At the gate level, DYY exhibited a significant impact on the abundance of Bacteroidota and Firmicutes in ALI rats, as well as on the regulation of genera such as Ruminococcus, Lactobacillus and Romboutsia. Additionally, cecal metabonomics analysis revealed that DYY effectively modulated the abnormal expression of 12 key metabolic biomarkers in ALI rats, thereby promoting intestinal homeostasis through pathways such as Purine metabolism. Furthermore, Pearson analysis indicated a strong correlation between the dysregulation of intestinal microbiota, differential metabolites and inflammation. These findings preliminarily confirm that ALI is closely related to the disorder of cecal microbial and metabolic, and DYY can play a protective role by regulating this imbalance, which provides a new understanding of the multi-system linkage mechanism of DYY improving ALI.

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

PROVIDER: MTBLS10741 | MetaboLights | 2024-09-20

REPOSITORIES: MetaboLights

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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.

			Action	DRS
	NEG_Con1.mgf	Mgf
	NEG_Con2.mgf	Mgf
	NEG_Con3.mgf	Mgf
	NEG_Con4.mgf	Mgf
	NEG_Con5.mgf	Mgf

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Combined analysis of cecal microbiota and metabolomics reveals the intervention mechanism of Dayuan Yin in acute lung injury

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