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GHS-R1a deficiency mitigates lipopolysaccharide-induced lung injury in mice via the downregulation of macrophage activity.
Tanida, Ryota; Tsubouchi, Hironobu; Yanagi, Shigehisa; Saito, Yusuke; Toshinai, Koji; Miyazaki, Taiga; Takamura, Toshinari; Nakazato, Masamitsu.
Afiliación
  • Tanida R; Department of Neurology, Respirology, Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan; Department of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikaw
  • Tsubouchi H; Department of Neurology, Respirology, Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan; Division of Respirology, Rheumatology, Infectious Diseases, and Neurology, Department of Internal Medicine, Faculty of
  • Yanagi S; Department of Neurology, Respirology, Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan; Division of Respirology, Rheumatology, Infectious Diseases, and Neurology, Department of Internal Medicine, Faculty of
  • Saito Y; Division of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
  • Toshinai K; Department of Sports and Fitness, Faculty of Wellness, Shigakkan University, 55 Nakoyama, Yokone, Obu, 474-8651, Japan.
  • Miyazaki T; Division of Respirology, Rheumatology, Infectious Diseases, and Neurology, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Kihara 5200, Kiyotake, Miyazaki, 889-1692, Japan.
  • Takamura T; Department of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
  • Nakazato M; Department of Neurology, Respirology, Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan; Division of Inter-Organ Communication Research Project, Frontier Science Research Center, University of Miyazaki, 5200
Biochem Biophys Res Commun ; 589: 260-266, 2022 01 22.
Article en En | MEDLINE | ID: mdl-34929449
ABSTRACT
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.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Regulación hacia Abajo / Macrófagos Peritoneales / Receptores de Ghrelina / Lesión Pulmonar Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Biochem Biophys Res Commun Año: 2022 Tipo del documento: Article
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Regulación hacia Abajo / Macrófagos Peritoneales / Receptores de Ghrelina / Lesión Pulmonar Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Biochem Biophys Res Commun Año: 2022 Tipo del documento: Article