Taenia crassiceps is a cestode parasite of wild and domestic animals that rarely affects humans; it has been widely used as an experimental model. The asexual proliferation by budding is a useful attribute of T. crassiceps cysticerci, which allows the various strains to be maintained indefinitely in the peritoneal cavity of inbred mice. Over the last 50 years, experimental results using larval and adult stages of T. crassiceps have yielded much information on the morphology, infectivity, proliferation dynamics, host immune response, endocrinological responses and vaccine research, all of which have contributed to our knowledge of cestode biology.
Cysticerci of Taenia crassiceps reproduce asexually by exogenous budding in the rodent intermediate host, and can experimentally develop to the adult stage within the small intestine of golden hamsters. In the present study, we report the loss of cysticercus infectivity for hamsters after maintaining the strain for 4 yr by consecutive peritoneal passage in mice. Larval infectivity was restored after a cysticercus from the WFU strain developed into a gravid tapeworm after being passaged through a dog. The eggs of this tapeworm were infective for mice, which subsequently developed cysticerci with renewed capability for infecting experimental hamsters. An in vitro evagination assay was also conducted using eleventh-generation WFU strain cysticerci, as well as second- and fourth-generation dog-derived cysticerci. Significantly higher (P < 0.0001) evagination was observed for 5-mo-old dog-derived and WFU infrapopulations when compared with respective evagination values for 9- and 12-mo-old infrapopulations. The extent of evagination was linked to the capacity of cysticerci to infect hamsters, so that greater evagination resulted in a higher infectivity for hamsters and vice versa.
Methoxychlor (MXC) and vinclozolin (VIN) are well-recognized endocrine disrupting chemicals known to alter epigenetic regulations and transgenerational inheritance; however, non-endocrine disruption endpoints are also important. Thus, we determined the effects of MXC and VIN on the dysregulation of gap junctional intercellular communication (GJIC) and activation of mitogen-activated protein kinases (MAPKs) in WB-F344 rat liver epithelial cells. Both chemicals induced a rapid dysregulation of GJIC at non-cytotoxic doses, with 30 min EC 50 values for GJIC inhibition being 10 mM for MXC and 126 mM for VIN. MXC inhibited GJIC for at least 24 h, while VIN effects were transient and GJIC recovered after 4 h. VIN induced rapid hyperphosphorylation and internalization of gap junction protein connexin43, and both chemicals also activated MAPK ERK1/2 and p38. Effects on GJIC were not prevented by MEK1/2 inhibitor, but by an inhibitor of phosphatidylcholine-specific phospholipase C (PC-PLC), resveratrol, and in the case of VIN, also, by a p38 inhibitor. Estrogen (ER) and androgen receptor (AR) modulators (estradiol, ICI 182,780, HPTE, testosterone, flutamide, VIN M2) did not attenuate MXC or VIN effects on GJIC. Our data also indicate that the effects were elicited by the parental compounds of MXC and VIN. Our study provides new evidence that MXC and VIN dysregulate GJIC via mechanisms involving rapid activation of PC-PLC occurring independently of ER-or AR-dependent genomic signaling. Such alterations of rapid intercellular and intracellular signaling events involved in regulations of gene expression, tissue development, function and homeostasis, could also contribute to transgenerational epigenetic effects of endocrine disruptors.
Experimental taeniid strobilae from Taenia solium and T. crassiceps (WFU strain) were incubated for 0-72 h in 0, 5 or 20 mM glucose solutions and further exposed for 15 min to the gap junction fluorochrome Lucifer Yellow. Frozen sections were obtained from each worm and observed under an epifluorescent microscope. Worm sections from strobilae incubated with glucose, revealed intense fluorescence in the base of the tegumentary surface, suggesting that this tissue behaves as a gap junction complex. Fluorescence intensity differences between control worms not exposed to glucose and worms incubated with glucose, were highly significant. The results demonstrate that under in vitro conditions, glucose is taken up along the whole strobilar tegument in both taeniid species, suggesting, that although taeniids attached to the duodenum probably take up most of their nutrients directly from the mucosal wall, the capacity for absorbing glucose along the tegumentary surface is always active and may increase the survival capacity of these intestinal worms by promoting glucose absorption at other points in the intestinal lumen.
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