Leptin Downregulates LPS-Induced Lung Injury: Role of Corticosterone and Insulin

Autor(es)

Landgraf, Maristella A. ^{[1, 2, 3]} ; Silva, Reinaldo C. ; Correa-Costa, Matheus ^[3] ; Hiyane, Meire I. ^[3] ; Carvalho, Maria Helena C. ^[1] ; Landgraf, Richardt G. ^{[1, 2]} ; Camara, Niels O. S. ^{[3, 4]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci 1, Dept Pharmacol, Lab Hypertens, BR-1524 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Lab Inflammat & Vasc Pharmacol, BR-05508 Sao Paulo - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Lab Transplantat Immunobiol, BR-1524 Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, Div Nephrol, Lab Clin & Expt Immunobiol, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY; v. 33, n. 3, p. 835-846, 2014.
• Citações Web of Science: 16

Resumo

Background/Aims: We investigated the effects of leptin in the development of lipopolysaccharide (LPS)-induced acute lung inflammation (ALI) in lean mice. Methods: Mice were administered leptin (1.0 mu g/g) or leptin (1.0 mu g/g) followed by LPS (1.5 mu g/g) intranasally. Additionally, some animals were given LPS (1.5 mu g/g) or saline intranasally alone, as a control. Tissue samples and fluids were collected six hours after instillation. Results: We demonstrated that leptin alone did not induce any injury. Local LPS exposure resulted in significant acute lung inflammation, characterized by a substantial increase in total cells, mainly neutrophils, in bronchoalveolar lavages (BAL). We also observed a significant lymphocyte influx into the lungs associated with enhanced lung expression of chemokines and cytokines (KC, RANTES, TNF-alpha, IFN-beta, GM-CSF and VEGF). LPS-induced ALI was characterized by the enhanced expression of ICAM-1 and iNOS in the lungs. Mice that received LPS showed an increase in insulin levels. Leptin, when administered prior to LPS instillation, abolished all of these effects. LPS induced an increase in corticosterone levels, and leptin potentiated this event. Conclusion: These data suggest that exogenous leptin may promote protection during sepsis, and downregulation of the insulin levels and upregulation of corticosterone may be important mechanisms in the amelioration of LPS-induced ALI.Copyright (c) 2014 S. Karger AG, Basel (AU)

• Processo FAPESP: 12/10512-6 - 15th Biennial Meeting of the European Society for Immunodeficiencies
• Beneficiário: Maristella de Almeida Vitta Landgraf
• Modalidade de apoio: Auxílio à Pesquisa - Reunião - Exterior
• Processo FAPESP: 12/51104-8 - Mecanismos envolvidos na redução da resposta inflamatória pulmonar aguda e alérgica, em ratos Wistar desnutridos intra-uterinamente
• Beneficiário: Maristella de Almeida Vitta Landgraf
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 12/02270-2 - Novos mecanismos celulares, moleculares e imunológicos das lesões renais agudas e crônicas: busca por novas estratégias terapêuticas
• Beneficiário: Niels Olsen Saraiva Câmara
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 10/01404-0 - Estudos in vivo e in vitro da participação da leptina em diferentes modelos de inflamação pulmonar: mediadores inflamatórios e vias de sinalização envolvidas
• Beneficiário: Richardt Gama Landgraf
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores