Progesterone induces mucosal immunity in a rodent model of human taeniosis by Taenia solium


Por: Escobedo G., Camacho-Arroyo I., Nava-Luna P., Olivos A., Pérez-Torres A., Leon-Cabrera S., Carrero J.C., Morales-Montor J.

Publicada: 1 ene 2011
Resumen:
More than one quarter of human world's population is exposed to intestinal helminth parasites. The Taenia solium tapeworm carrier is the main risk factor in the transmission of both human neurocysticercosis and porcine cysticercosis. Sex steroids play an important role during T. solium infection, particularly progesterone has been proposed as a key immunomodulatory hormone involved in susceptibility to human taeniosis in woman and cysticercosis in pregnant pigs. Thus, we evaluated the effect of progesterone administration upon the experimental taeniosis in golden hamsters (Mesocricetus auratus). Intact female adult hamsters were randomly divided into 3 groups: progesterone-subcutaneously treated; olive oil-treated as the vehicle group; and untreated controls. Animals were treated every other day during 4 weeks. After 2 weeks of treatment, all hamsters were orally infected with 4 viable T. solium cysticerci. After 2 weeks post infection, progesterone-treated hamsters showed reduction in adult worm recovery by 80%, compared to both vehicle-treated and non-manipulated infected animals. In contrast to control and vehicle groups, progesterone treatment diminished tapeworm length by 75% and increased proliferation rate of leukocytes from spleen and mesenteric lymph nodes of infected hamsters by 5-fold. The latter exhibited high expression levels of IL-4, IL-6 and TNF-a at the duodenal mucosa, accompanied with polymorphonuclear leukocytes infiltration. These results support that progesterone protects hamsters from the T. solium adult tapeworm establishment by improving the intestinal mucosal immunity, suggesting a potential use of analogues of this hormone as novel inductors of the gut immune response against intestinal helminth infections and probably other bowel-related disorders. © Ivyspring International Publisher.

Filiaciones:
Escobedo G.:
 Unidad de Medicina Experimental, Hospital General de México, México D.F. 06726, Mexico

Camacho-Arroyo I.:
 Univ Nacl Autonoma Mexico, Fac Quim, Dept Biol, Mexico City 04510, DF, Mexico

Nava-Luna P.:
 Univ Nacl Autonoma Mexico, Dept Inmunol, Inst Invest Biomed, Mexico City 04510, DF, Mexico

Olivos A.:
 Univ Nacl Autonoma Mexico, Hosp Gen Mexico, Dept Expt Med, Fac Med, Mexico City 06726, DF, Mexico

Pérez-Torres A.:
 Univ Nacl Autonoma Mexico, Fac Med, Dept Biol Celular & Tisular, Mexico City 04510, DF, Mexico

Leon-Cabrera S.:
 Univ Nacl Autonoma Mexico, Fac Med, Dept Microbiol & Parasitol, Mexico City 04510, DF, Mexico

Carrero J.C.:
 Univ Nacl Autonoma Mexico, Dept Inmunol, Inst Invest Biomed, Mexico City 04510, DF, Mexico

Morales-Montor J.:
 Univ Nacl Autonoma Mexico, Dept Inmunol, Inst Invest Biomed, Mexico City 04510, DF, Mexico
ISSN: 14492288
Editorial
IVYSPRING INT PUBL, PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA, Australia
Tipo de documento: Article
Volumen: 7 Número: 9
Páginas: 1443-1456
WOS Id: 000298011000020
ID de PubMed: 22110394
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