Lipopolysaccharides (LPS) is an endotoxin derived from the outer leaflet of the outer membrane of Gram-negative bacteria. Lipopolysaccharides consists of an antigen O-specific chain, a core oligosaccharide and lipid A. Lipopolysaccharides is a pathogenic associated molecular pattern (PAMP) that activates the immune system. Lipopolysaccharides activates TLR-4 on immune cells[1][2][3]. This product is derived from Escherichia coli O55:B5.
Lipopolysaccharides (10-80 μg/mL) selectively decreases THir (tyrosine hydroxylase immunoreactive) cells and increases culture media levels of interleukin1β (IL-1β) and tumor necrosis factor-α (TNF-α) as well as nitrite (an index of nitric oxide (NO) production)[4].
Lipopolysaccharides (1.5 mg/kg; i.p.; once) induces sickness and hypothermia in mice, and induces a greater and more prolonged sickness response in adult male mice[3].
| Animal Model: | Female and male CD1 mice[3] |
| Dosage: | 1.5mg/kg |
| Administration: | Intraperitoneal injection, once |
| Result: | Induced sickness behavior in all mice, but adult mice displayed more sickness than pubertal mice and adult males remained sick for a longer period of time than adult females. Caused a decrease in body temperature for all mice, but this decrease was greatest in adult males. Increased pro- and anti-inflammatory cytokines at various levels in pubertal and adult male and female mice, resulted in age and sex differences in cytokine concentrations following immune challenge. Only adult males and females treated with LPS displayed significantly more IL-6 than their saline controls, and pubertal males and females and adult females displayed significantly more IL-10 than their saline controls. All the mice displayed significantly more IL-12 and TNF-α than their saline controls. |