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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

Full text
Author(s):
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]
Total Authors: 7
Affiliation:
[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
Total Affiliations: 4
Document type: Journal article
Source: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY; v. 33, n. 3, p. 835-846, 2014.
Web of Science Citations: 16
Abstract

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)

FAPESP's process: 12/10512-6 - 15th Biennial Meeting of the European Society for Immunodeficiencies
Grantee:Maristella de Almeida Vitta Landgraf
Support Opportunities: Research Grants - Meeting - Abroad
FAPESP's process: 12/51104-8 - Mechanisms involved in reduced acute and allergic lung inflammation in rats exposed to intrauterine undernourishment.
Grantee:Maristella de Almeida Vitta Landgraf
Support Opportunities: Research Grants - Young Investigators Grants
FAPESP's process: 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches
Grantee:Niels Olsen Saraiva Câmara
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 10/01404-0 - In vivo and in vitro studies of the leptin role in different models of lung inflammation: inflammatory mediators and signaling airways participation
Grantee:Richardt Gama Landgraf
Support Opportunities: Research Grants - Young Investigators Grants