Metabolic profile of the liver of mice infected with cysticerci of Taenia crassiceps

Abstract

Proton nuclear magnetic resonance (NMR) spectra of liver extracts from mice infected with cysticerci of Taenia crassiceps for 84 or 200 days showed differences in the concentrations of liver metabolites as compared with those of normal liver. The livers of mice infected for 84 days contained less glycogen and β-hydroxybutyrate but more glycine, taurine, betaine, phosphocholine (PC), choline, alanine and lactate. At 200 days post-infection (p.i.) the levels of hepatic glycogen and β-hydroxybutyrate remained lower and those of taurine, PC, choline, alanine and lactate were still elevated, but the concentration of glycine fell below that seen in the 84-day group and that of betaine assumed a value not statistically different from that of either the controls or the 84-day group. The concentrations of glucose, glycerophosphocholine, acylcarnitine, succinate and acetate stayed unchanged throughout the experiment.& b d y : During their existence in the mammalian host, cysticerci of Taenia crassiceps successfully resist the immunological responses of the host and induce various histopathological manifestations (Freeman 1964;Chernin and McLaren 1983;Bojail et al. 1993). As they proliferate in the peritoneal cavity, their demand for nutrients increases, which results in a pronounced loss of the host's net body weight (Crompton et al. 1985) and its eventual death. To explore further the consequences of nutrient competition in this host-parasite system we examined, utilizing nuclear magnetic resonance (NMR) spectroscopy, the influence of cysticerci on liver metabolism in the mouse host.A total of 20 Swiss-Webster female mice aged 3 months were inoculated intraperitoneally with 0.5 ml of packed T. crassiceps metacestodes each. Ten uninfected mice served as controls. Half of the infected mice were dissected on day 84 of the infection and the other half were killed at 200 days post-infection (p.i.). At the time of dissection the mice were anaesthetized intramuscularly with pentobarbital (60 mg/kg), after which their abdomens were opened and their livers, excised. The organs and the cysticerci collected from the peritoneal cavity of infected mice were rinsed in saline, weighed and immediately frozen in liquid N 2 . All samples were kept at -70°C until extracted and prepared for NMR analysis according to the method described by Blackburn et al. (1993) except that each sample was resuspended in 1.3 ml D 2 O. A known amount of sodium [2, 2, 3, 3-2 H 4 ]-3-trimethylsilylpropionate (TSP) was added as a chemical shift and intensity standard. The 1 H-NMR spectra of extracts were obtained with a Bruker AMX-500 NMR spectrometer using the acquisition parameters previously described by Novak et al. (1992); peak assignments and the method of quantitative measurement are also discussed therein. Data were analyzed statistically using analysis of variance (ANOVA). An α value of ≤0.05 was deemed significant.The livers of mice infected for 84 days contained less glycogen (the values indicate the concentration in micromoles of glucose units havin...

Changes in hepatic lipids of mice infected with cysticerci ofTaenia crassiceps

“…With the reduction in the amount of FA found in the liver of infected animals, it can be assumed that FAs are no longer available in excess to be channelled into ketogenic processes. The lower concentration of hepatic b-hydroxybutyrate in mice infected with T. crassiceps (Corbin et al, 1996) supports this hypothesis. It seems then that the FAs available in the liver were used for energy generation; continued complete oxidation of FA is essential for this organ as it derives most of its energy from this process (Seifter & Englard, 1994).…”

“…In addition to the removal of FAs, the cysticerci also acquire substantial amounts of glucose from the host. In response, the liver attempts to correct this metabolic disturbance by mobilizing glycogen stores and accelerating the gluconeogenic process (Corbin et al, 1996(Corbin et al, , 1999. As a consequence, the utilization of glucose in secondary pathways, such as FA synthesis, is inhibited (Goodridge et al, 1986;Katz, 1986;Sugden et al, 1993).…”

“…During their existence in the mammalian host, cysticerci remove considerable amounts of nutrients and by doing so induce various metabolic disorders. In murine cysticercosis, carbohydrate metabolism is severly altered resulting in an increased rate of gluconeogenesis in the liver of infected animals (Corbin et al, 1996(Corbin et al, , 1999. In addition, host body fat content was found to be signi®cantly reduced (Crompton et al, 1985).…”

Behavioural dominance and Taenia crassiceps parasitism in BALB/c male mice

“…In addition, these authors demonstrated a 200-fold increase of 17 b-oestradiol, involving a feminization of T. crassicepsinfected male mice. The cysticerci of T. crassiceps could also be involved in the disruption of mouse food intake (Crompton et al 1985;Corbin et al 1996;2000), as well as affecting the immunological system of the mouse host (Huerta et al 1992;Terrazas et al 1994Terrazas et al , 1999Villa and Kuhn 1996;Toenjes et al 1999). Under these circumstances, it was not surprising that T. crassiceps infection led to modification of the antagonistic behaviour and dominance status of male mice.…”

Multiple infestations of gastrointestinal parasites – Probable cause for high mortality of Spot-billed Pelican (Pelecanus philippensis) at Kokrebellur Community Reserve, India

“…The parasite transmission mode, lethality of the infection, and the life history traits are decided by the parasites (Poulin et al, 2011). Even when the parasite is in sub-lethal level, it can cause damage to the host by taking partial control over the behaviour such as changes in locomotion, light sensitivity, pain threshold, disruption of food intake, even affecting the immunological system of the host (Holmes and Bethel, 1972; Crompton et al, 1985; Huerta et al, 1992; Poulin, 1994; Thompson and Kavaliers, 1994; Corbin et al, 1996; Kavaliers et al, 1999). The parasitic infections in aquatic birds are one of the major threats to their populations along with factors including human disturbances at the nesting sites and wetlands, deforestation (Subramanya, 2006; Taher, 2007), hunting (Talukdar, 1999), and poaching of eggs and chicks (Talukdar, 1999; Chandrasekhar, 2009).…”