| First Author | Tanida R | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 589 |
| Pages | 260-266 | PubMed ID | 34929449 |
| Mgi Jnum | J:319768 | Mgi Id | MGI:6865199 |
| Doi | 10.1016/j.bbrc.2021.12.044 | Citation | Tanida R, et al. (2022) GHS-R1a deficiency mitigates lipopolysaccharide-induced lung injury in mice via the downregulation of macrophage activity. Biochem Biophys Res Commun 589:260-266 |
| abstractText | Acute respiratory distress syndrome (ARDS) is a critical illness syndrome characterized by dysregulated pulmonary inflammation. Currently, effective pharmacological treatments for ARDS are unavailable. Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor type 1a (GHS-R1a), has a pivotal role in regulating energy metabolism and immunomodulation. The role of endogenous ghrelin in ARDS remains unresolved. Herein, we investigated the role of endogenous ghrelin signaling by using GHS-R1a-null (ghsr(-/-)) mice and lipopolysaccharide (LPS)-induced ARDS model. Ghsr(-/-) mice survived longer than controls after LPS-induced lung injury. Ghsr(-/-) mice showed lower levels of pro-inflammatory cytokines and higher oxygenation levels after lung injury. The peritoneal macrophages isolated from ghsr(-/-) mice exhibited lower levels of cytokines production and oxygen consumption rate after LPS stimulation. Our results indicated that endogenous ghrelin plays a pivotal role in initiation and continuation in acute inflammatory response in LPS-induced ARDS model by modulating macrophage activity, and highlighted endogenous GHS-R1a signaling in macrophage as a potential therapeutic target in this relentless disease. |
