Hymenolepis diminuta: Activity of anti-oxidant enzymes in different parts of rat gastrointestinal tract

The antioxidant defence mechanisms of parasite and host after chronic Hymenolepis diminuta infestation of the rat

“…Similar results were also reported by other authors (Kosik-Bogacka et al 2011). Now we obtained especially important and valuable results in parasite-host setting concerning the influence of long-term H. diminuta parasitosis on the antioxidant system in definitive host intestine, and simultaneously showing a defense strategy of parasite against oxidative stress.…”

Changes of enzymatic antioxidant system in the small intestine of rats after the chronic invasion by Hymenolepis diminuta (Cestoda, Hymenolepididae)

“…Results obtained in this study confirm also recently published data, indicating that in the course of H. diminuta invasion, impairment of anti-oxidative defense mechanisms occurs in the small intestine of rat, which may cause changes typical for parasitic invasions (Shin et al, 2009;Kosik-Bogacka et al, 2011).…”

“…H. diminuta invasions are mild, without clear clinical symptoms (Milazzo et al, 2010). However experimental research performed in rats demonstrates that these invasions are accompanied by pathological changes in the mucous membrane of small intestine, such as: inflammatory infiltrations, flattening and shortening of intestinal villi, absorption disturbances, ion transport disturbances (Mettrick, 1980;Fal & Czaplicka, 1991;Starke & Oaks, 2001;Kosik-Bogacka et al, 2010). In invaded rats the following effects were noted in small intestine: higher number of mucous cells, compromised intestinal motility and decreased rate of bowel transit.…”

Hymenolepis diminuta: Analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats. Part II

“…In our previous studies, we observed that experimental hymenolepidosis was accompanied by changes in the activity of anti-oxidative enzymes and in concentrations of reduced glutathione as a result of oxidative stress (Kosik-Bogacka et al, 2011b). T. gondii-derived heat shock protein 70 (rTgHSP70) signaling mechanisms were mediated by TLR2, myeloid differentiation factor 88 (MyD88) and IL-1R-associated kinase (IRAK4), but not by TLR4.…”