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Single cell RNA sequencing of lung myeloid cells from aged (20-22 months old) mice treated with Isotype or anti-IFNAR1 antibody for 1 day or 1 week

ABSTRACT: Monocytes and neutrophils are an important subset of myeloid cells in the lung. However, little is known about how aging affects these lung cells, and the role of Type I interferon signaling. Here, we treat aged (20-22 months old) mice with 500ug anti-IFNAR1 antibody (Clone MAR1-5A3 from BioXcell) intraperitoneally (i.p.) once or for 1 week (total 4 i.p. injections, one every other day) and sorted CD45+ CD11b+ Gr1+ cells from the lung the day after the last injection. We performed single cell RNA sequencing to identify the role of Type I Interferon in these cells from the aging mouse lung.

ORGANISM(S): Mus musculus

PROVIDER: GSE167170 | GEO | 2021/10/20

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 of lung myeloid cells from aged (20-22 months old) mice treated with Isotype or anti-IFNAR1 antibody for 1 day or 1 week

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