1. Bovine dialyzable leukocyte extract protects against LPS-induced, murine endotoxic shock.
- Author
-
Franco-Molina MA, Mendoza-Gamboa E, Castillo-León L, Tamez-Guerra RS, and Rodríguez-Padilla C
- Subjects
- Animals, Cattle, Cytokines classification, Cytokines genetics, Cytokines immunology, Dose-Response Relationship, Drug, Endotoxins antagonists & inhibitors, Inflammation genetics, Inflammation immunology, Inflammation Mediators immunology, Inflammation Mediators metabolism, Injections, Intraperitoneal, Leukocytes immunology, Mexico, Mice, Mice, Inbred BALB C, Shock, Septic chemically induced, Transfer Factor pharmacology, Endotoxins adverse effects, Lipopolysaccharides adverse effects, Lipopolysaccharides antagonists & inhibitors, Shock, Septic mortality, Shock, Septic prevention & control, Transfer Factor therapeutic use
- Abstract
The pathophysiology of endotoxic shock is characterized by the activation of multiple pro-inflammatory genes and their products which initiate the inflammatory process. Endotoxic shock is a serious condition with high mortality. Bovine dialyzable leukocyte extract (bDLE) is a dialyzate of a heterogeneous mixture of low molecular weight substances released from disintegrated leukocytes of the blood or lymphoid tissue obtained from homogenized bovine spleen. bDLE is clinically effective for a broad spectrum of diseases. To determine whether bDLE improves survival and modulates the expression of pro-inflammatory cytokine genes in LPS-induced, murine endotoxic shock, Balb/C mice were treated with bDLE (1 U) after pretreatment with LPS (17 mg/kg). The bDLE improved survival (90%), suppressed IL-10 and IL-6, and decreased IL-1beta, TNF-alpha, and IL-12p40 mRNA expression; and decreased the production of IL-10 (P<0.01), TNF-alpha (P<0.01), and IL-6 (P<0.01) in LPS-induced, murine endotoxic shock. Our results demonstrate that bDLE leads to improved survival in LPS-induced endotoxic shock in mice, modulating the pro-inflammatory cytokine gene expression, suggesting that bDLE is an effective therapeutic agent for inflammatory illnesses associated with an unbalanced expression of pro-inflammatory cytokine genes such as in endotoxic shock, rheumatic arthritis and other diseases.
- Published
- 2004
- Full Text
- View/download PDF