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Single-cell RNA sequencing reveals Reg3g-dependent alteration of alveolar macrophage transcriptomes during LPS-induced acute lung injury

ABSTRACT: To investigate how Reg3g modulates alveolar macrophage (AM) transcriptional programs during acute lung injury, we performed single-cell RNA sequencing on fluorescence-activated cell sorting (FACS)-purified CD45⁺Ly6G⁻F4/80⁺CD11b/c⁺ lung macrophages from mice treated with PBS, LPS, or LPS + Reg3g for 24 hours. Libraries were generated using the 10x Genomics Chromium GEM-X Single Cell 3′ platform. Following quality control, approximately 29,000 cells were retained. Unsupervised clustering identified 22 distinct cell populations. Reclustering of AMs revealed multiple transcriptional states. LPS exposure shifted AMs toward a pro-inflammatory phenotype, whereas Reg3g treatment attenuated this inflammatory remodeling and restored homeostatic transcriptional signatures. These data identify Reg3g as a modulator of alveolar macrophage functional plasticity during acute lung injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE332959 | GEO | 2026/06/01

REPOSITORIES: GEO

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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.

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Single-cell RNA sequencing reveals Reg3g-dependent alteration of alveolar macrophage transcriptomes during LPS-induced acute lung injury

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