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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.)

Immune cells and oxidative stress in the endotoxin tolerance mouse model

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Author(s):
Melo, E. S. [1] ; Barbeiro, H. V. [1] ; Ariga, S. [1] ; Goloubkova, T. [1] ; Curi, R. [2] ; Velasco, I. T. [1] ; Vasconcelos, D. [3] ; Soriano, F. G. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Fac Med, Disciplina Emergencias Clin, Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Ciencias Biomed, Dept Fisiol & Biofis, Sao Paulo - Brazil
[3] Univ Sao Paulo, Inst Trop Med, Dept Dermatol, Lab Invest Dermatol & Imunodeficiencia, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 43, n. 1, p. 57-67, JAN 2010.
Web of Science Citations: 15
Abstract

Sepsis is a systemic inflammatory response that can lead to tissue damage and death. In order to increase our understanding of sepsis, experimental models are needed that produce relevant immune and inflammatory responses during a septic event. We describe a lipopolysaccharide tolerance mouse model to characterize the cellular and molecular alterations of immune cells during sepsis. The model presents a typical lipopolysaccharide tolerance pattern in which tolerance is related to decreased production and secretion of cytokines after a subsequent exposure to a lethal dose of lipopolysaccharide. The initial lipopolysaccharide exposure also altered the expression patterns of cytokines and was followed by an 8- and a 1.5-fold increase in the T helper 1 and 2 cell subpopulations. Behavioral data indicate a decrease in spontaneous activity and an increase in body temperature following exposure to lipopolysaccharide. In contrast, tolerant animals maintained production of reactive oxygen species and nitric oxide when terminally challenged by cecal ligation and puncture (CLP). Survival study after CLP showed protection in tolerant compared to naive animals. Spleen mass increased in tolerant animals followed by increases of B lymphocytes and subpopulation Th1 cells. An increase in the number of stem cells was found in spleen and bone marrow. We also showed that administration of spleen or bone marrow cells from tolerant to naive animals transfers the acquired resistance status. In conclusion, lipopolysaccharide tolerance is a natural reprogramming of the immune system that increases the number of immune cells, particularly T helper 1 cells, and does not reduce oxidative stress. (AU)