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      Progesterone Induces Mucosal Immunity in a Rodent Model of Human Taeniosis by Taenia solium

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          Abstract

          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-α 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.

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          Most cited references79

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          Hormonal and immunological mechanisms mediating sex differences in parasite infection.

          S L Klein (2004)
          The prevalence and intensity of infections caused by protozoa, nematodes, trematodes, cestodes, and arthropods is higher in males than females. The primary thesis of this review is that immunological differences exist between the sexes that may underlie increased parasitism in males compared to females. Several field and laboratory studies link sex differences in immune function with circulating steroid hormones; thus, the roles of sex steroids, including testosterone, oestradiol, and progesterone, as well as glucocorticoids will be discussed. Not only can host hormones affect responses to infection, but parasites can both produce and alter hormone concentrations in their hosts. The extent to which changes in endocrine-immune interactions following infection are mediated by the host or the parasite will be considered. Although males are more susceptible than females to many parasites, there are parasites for which males are more resistant than females and endocrine-immune interactions may underlie this sex reversal. Finally, although immunological differences exist between the sexes, genetic and behavioural differences may explain some variability in response to infection and will be explored as alternative hypotheses for how differences between the sexes contribute to dimorphic responses to parasites.
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            Neurocysticercosis: updated concepts about an old disease.

            Neurocysticercosis, the infection of the human brain by the larvae of Taenia solium, is a major cause of acquired epilepsy in most low-income countries. Cases of neurocysticercosis are becoming more common in high-income countries because of increased migration and travel. Diagnosis by neuroimaging and serological assessment has greatly improved over the past decade, and the natural progression of the disease and response to antiparasitic drugs is now much better understood. Neurocysticercosis is potentially eradicable, and control interventions are underway to eliminate this infection. Meanwhile, updated information on diagnosis and management of neurocysticercosis is required, especially for clinicians who are unfamiliar with its wide array of clinical presentations.
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              Estradiol activates mast cells via a non-genomic estrogen receptor-alpha and calcium influx.

              Allergic airway diseases are more common in females than in males during early adulthood. A relationship between female hormones and asthma prevalence and severity has been suggested, but the cellular and molecular mechanisms are not understood. To elucidate the mechanism(s) by which estrogens enhance the synthesis and release of mediators of acute hypersensitivity. Two mast cell/basophil cell lines (RBL-2H3 and HMC-1) and primary cultures of bone marrow derived mast cells, all of which naturally express estrogen receptor-alpha, were examined. Cells were incubated with physiological concentrations of 17-beta-estradiol with and without IgE and allergens. Intracellular Ca(2+) concentrations and the release of beta-hexosaminidase and leukotriene C(4) were quantified. Estradiol alone induced partial release of the preformed, granular protein beta-hexosaminidase from RBL-2H3, BMMC and HMC-1, but not from BMMC derived from estrogen receptor-alpha knock-out mice. The newly synthesized LTC(4) was also released from RBL-2H3. Estradiol also enhanced IgE-induced degranulation and potentiated LTC(4) production. Intracellular Ca(2+) concentration increased prior to and in parallel with mediator release. Estrogen receptor antagonists or Ca(2+) chelation inhibited these estrogenic effects. Binding of physiological concentrations of estradiol to a membrane estrogen receptor-alpha initiates a rapid onset and progressive influx of extracellular Ca(2+), which supports the synthesis and release of allergic mediators. Estradiol also enhances IgE-dependent mast cell activation, resulting in a shift of the allergen dose response.
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                Author and article information

                Journal
                Int J Biol Sci
                ijbs
                International Journal of Biological Sciences
                Ivyspring International Publisher (Sydney )
                1449-2288
                2011
                10 November 2011
                : 7
                : 9
                : 1443-1456
                Affiliations
                1. Unidad de Medicina Experimental, Hospital General de México, México D.F. 06726, México.
                2. Facultad de Química, Departamento de Biología, Universidad Nacional Autónoma de México, México D.F. 04510, México.
                3. Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México D.F. 04510, México.
                4. Departamento de Medicina Experimental, Facultad de Medicina, Hospital General de México, Universidad Nacional Autónoma de México, México D.F. 06726, México.
                5. Departamento de Biología Celular y Tisular, Facultad de Medicina, Universidad Nacional Autónoma de México, México D.F. 04510, México.
                6. Departamento de Microbiología y Parasitología, Facultad de Medicina, Universidad Nacional Autónoma de México, México D.F. 04510, México.
                Author notes
                ✉ Corresponding author: Jorge Morales-Montor Ph.D. Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, AP 70228, México D.F. 04510, México. Telephone 0052(55)-5622-3854, Fax 0052(55) 5622-3369. E-mail: jmontor66@ 123456biomedicas.unam.mx

                Conflict of Interests: The authors have declared that no conflict of interest exists.

                Article
                ijbsv07p1443
                3221950
                22110394
                24cd6fb4-2212-46ae-807d-1014c041c1a1
                © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                History
                : 1 October 2011
                : 26 October 2011
                Categories
                Research Paper

                Life sciences
                sex hormones,progesterone,inflammation.,taenia solium,cysticercosis
                Life sciences
                sex hormones, progesterone, inflammation., taenia solium, cysticercosis

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