A helminth cestode parasite express an estrogen-binding protein resembling a classic nuclear estrogen receptor

Ibarra-Coronado, Elizabeth; Escobedo, Galileo; Nava-Castro, Karen Elizabeth; Ramses, Chávez-Rios Jesús; Hernández-Bello, Romel; García-Varela, Martìn; Ambrosio, Javier R.; Reynoso-Ducoing, Olivia; Fonseca-Liñán, Rocío; Ortega‐Pierres, Guadalupe; Pavón, Lenin; Hernández, Marı́a Eugenia; Morales‐Montor, Jorge

doi:10.1016/j.steroids.2011.05.003

Cited by 27 publications

(16 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[AcB55xDBA/2] F1 hybrids and 379 [AcB55xDBA/2] F2 animals were infected intraperitoneally with 10 non-budding T. crassiceps larvae in three separate infections, and parasite burden was measured 30 days later (Figure 4A). Due to the previously reported gender-associated differential permissiveness to T. crassiceps , where higher concentrations of estrogen and estradiol are concomitant with increased parasite burdens [17], [18] typically occurring in female mice, we segregated males and females in the analysis (Figure 4A). Both male and female [AcB55xDBA/2] F1 hybrids were fully resistant with parasite load similar to the AcB55 controls (Figure 4A), suggesting that resistance to T. crassiceps is inherited in a dominant fashion.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Identification of Loci Controlling Restriction of Parasite Growth in Experimental Taenia crassiceps Cysticercosis

et al. 2011

View full text Add to dashboard Cite

Human neurocysticercosis (NC) caused by Taenia solium is a parasitic disease of the central nervous system that is endemic in many developing countries. In this study, a genetic approach using the murine intraperitoneal cysticercosis caused by the related cestode Taenia crassiceps was employed to identify host factors that regulate the establishment and proliferation of the parasite. A/J mice are permissive to T. crassiceps infection while C57BL/6J mice (B6) are comparatively restrictive, with a 10-fold difference in numbers of peritoneal cysticerci recovered 30 days after infection. The genetic basis of this inter-strain difference was explored using 34 AcB/BcA recombinant congenic strains derived from A/J and B6 progenitors, that were phenotyped for T. crassiceps replication. In agreement with their genetic background, most AcB strains (A/J-derived) were found to be permissive to infection while most BcA strains (B6-derived) were restrictive with the exception of a few discordant strains, together suggesting a possible simple genetic control. Initial haplotype association mapping using >1200 informative SNPs pointed to linkages on chromosomes 2 (proximal) and 6 as controlling parasite replication in the AcB/BcA panel. Additional linkage analysis by genome scan in informative [AcB55xDBA/2]F1 and F2 mice (derived from the discordant AcB55 strain), confirmed the effect of chromosome 2 on parasite replication, and further delineated a major locus (LOD = 4.76, p<0.01; peak marker D2Mit295, 29.7 Mb) that we designate Tccr1 (T. crassiceps cysticercosis restrictive locus 1). Resistance alleles at Tccr1 are derived from AcB55 and are inherited in a dominant fashion. Scrutiny of the minimal genetic interval reveals overlap of Tccr1 with other host resistance loci mapped to this region, most notably the defective Hc/C5 allele which segregates both in the AcB/BcA set and in the AcB55xDBA/2 cross. These results strongly suggest that the complement component 5 (C5) plays a critical role in early protective inflammatory response to infection with T. crassiceps.

show abstract

Section: Resultsmentioning

confidence: 99%

“…Finally, clear differences between the parasite load of male and female have been noted in inbred mouse strains [16]. Females show higher numbers of cysticerci compared to males due to a significant effect of sex hormones on response to infection [17], [18].…”

Section: Introductionmentioning

confidence: 99%

Identification of Loci Controlling Restriction of Parasite Growth in Experimental Taenia crassiceps Cysticercosis

et al. 2011

View full text Add to dashboard Cite

show abstract

“…The chemical structure of the steroids may favour any effective interaction with the tegumental surface. We recently described an oestrogen receptor on the tegument of the parasite [37]. Thus, androgens can bind to a steroid hormone receptor and interact with the surface of parasites, as deep cells of the germinal zones do with flame cells.…”

Section: Discussionmentioning

confidence: 99%

Androgens Exert a Cysticidal Effect upon Taenia crassiceps by Disrupting Flame Cell Morphology and Function

et al. 2015

Self Cite

View full text Add to dashboard Cite

The effects of testosterone (T4) and dihydrotestosterone (DHT) on the survival of the helminth cestode parasite Taenia crassiceps, as well as their effects on actin, tubulin and myosin expression and their assembly into the excretory system of flame cells are described in this paper. In vitro evaluations on parasite viability, flow cytometry, confocal microscopy, video-microscopy of live flame cells, and docking experiments of androgens interacting with actin, tubulin, and myosin were conducted. Our results show that T4 and DHT reduce T. crassiceps viability in a dose- and time-dependent fashion, reaching 90% of mortality at the highest dose used (40 ng/ml) and time exposed (10 days) in culture. Androgen treatment does not induce differences in the specific expression pattern of actin, tubulin, and myosin isoforms as compared with control parasites. Confocal microscopy demonstrated a strong disruption of the parasite tegument, with reduced assembly, shape, and motion of flame cells. Docking experiments show that androgens are capable of affecting parasite survival and flame cell morphology by directly interacting with actin, tubulin and myosin without altering their protein expression pattern. We show that both T4 and DHT are able to bind actin, tubulin, and myosin affecting their assembly and causing parasite intoxication due to impairment of flame cell function. Live flame cell video microscopy showing a reduced motion as well changes in the shape of flame cells are also shown. In summary, T4 and DHT directly act on T. crassiceps cysticerci through altering parasite survival as well as the assembly and function of flame cells.

show abstract

“…Our current understanding of the relationship between hormones and parasite infection suggests that parasites can synthesize proteins, such as receptors with the ability to bind host hormones, and cause downstream transcriptional gene activation. As a result, parasites can positively or negatively affect the course of infection [6,7]. Based on the above data, this review examines how hormones effect on the immune system and their implications in parasite infections.…”

Section: Hormones and Parasitesmentioning

confidence: 99%

Endocrine Immune Interactions in the Host-Parasite Relationship: Steroid Hormones as Immune Regulators in Parasite Infections

H¹,

KE²

2015

J Steroids Hormon Sci

View full text Add to dashboard Cite

A helminth cestode parasite express an estrogen-binding protein resembling a classic nuclear estrogen receptor

Cited by 27 publications

References 28 publications

Identification of Loci Controlling Restriction of Parasite Growth in Experimental Taenia crassiceps Cysticercosis

Identification of Loci Controlling Restriction of Parasite Growth in Experimental Taenia crassiceps Cysticercosis

Androgens Exert a Cysticidal Effect upon Taenia crassiceps by Disrupting Flame Cell Morphology and Function

Endocrine Immune Interactions in the Host-Parasite Relationship: Steroid Hormones as Immune Regulators in Parasite Infections

Contact Info

Product

Resources

About