Adiponectin (Acrp30) is an insulin-sensitizing hormone with beneficial effects on a number of biological and metabolic processes by two widely expressed receptors, AdipoR1 and AdipoR2. To date, the role of Acrp30 in lung is not completely assessed but altered levels of Acrp30 and modulated expression of both AdipoRs have been described in Chronic Obstructive Pulmonary disease (COPD) (1). Lung inflammation, a crucial component of COPD progression, is mainly sustained by two potent pro-inflammatory cytokines: Tumor Necrosis Factor α (TNFα) and Interleukin 1β (IL-1β). These mediators in turn propagate and perpetuate the inflammation also through NF-κB, a transcriptional factor for many genes involved in inflammation, injury and stress in lung. In this study we analyzed the effects of Acrp30 on human alveolar epithelial cell line (A549) selected as an in vitro model of lung epithelia. We treated A549 cells with TNFα or IL-1β and visualized the NF-κB nuclear transactivation by confocal microscopy. Successively, we evaluated the role of Acrp30 in this process: we treated the cells with Acrp30 and subsequently with TNFα or IL-1β and analyzed NF-κB nuclear transactivation. Finally, we investigated by western blotting the phosphorylation status of ERK1/2 kinase, one of the main molecules involved in Acrp30 signal pathway. A better elucidation of the Acrp30 role in the control of local lung inflammatory state may contribute to develop new therapeutic approaches in inflammatory diseases as COPD, a major cause of morbidity and death worldwide

Anti-inflammatory effects of adiponectin in A549 cells exposed to TNF alpha and IL-1 beta

Nigro E;BIANCO, Andrea;DANIELE, Aurora
2012

Abstract

Adiponectin (Acrp30) is an insulin-sensitizing hormone with beneficial effects on a number of biological and metabolic processes by two widely expressed receptors, AdipoR1 and AdipoR2. To date, the role of Acrp30 in lung is not completely assessed but altered levels of Acrp30 and modulated expression of both AdipoRs have been described in Chronic Obstructive Pulmonary disease (COPD) (1). Lung inflammation, a crucial component of COPD progression, is mainly sustained by two potent pro-inflammatory cytokines: Tumor Necrosis Factor α (TNFα) and Interleukin 1β (IL-1β). These mediators in turn propagate and perpetuate the inflammation also through NF-κB, a transcriptional factor for many genes involved in inflammation, injury and stress in lung. In this study we analyzed the effects of Acrp30 on human alveolar epithelial cell line (A549) selected as an in vitro model of lung epithelia. We treated A549 cells with TNFα or IL-1β and visualized the NF-κB nuclear transactivation by confocal microscopy. Successively, we evaluated the role of Acrp30 in this process: we treated the cells with Acrp30 and subsequently with TNFα or IL-1β and analyzed NF-κB nuclear transactivation. Finally, we investigated by western blotting the phosphorylation status of ERK1/2 kinase, one of the main molecules involved in Acrp30 signal pathway. A better elucidation of the Acrp30 role in the control of local lung inflammatory state may contribute to develop new therapeutic approaches in inflammatory diseases as COPD, a major cause of morbidity and death worldwide
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11591/210320
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 0
social impact