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ABSTRACT: Mating shut down a 2-methoxyestradiol (2ME) nongenomic action necessary to accelerate egg transport in the rat oviduct. Herein we investigated whether TNF-α participates in this mating effect. In unmated and mated rats, we determined the concentration of TNF-α in the oviductal fluid and the level of the mRNA for Tnfa and their receptors Tnfrsf1a and Tnfrsf1b in the oviduct tissues. The distribution of the TNFRSF1A and TNFRSF1B proteins in the oviduct of unmated and mated was also assessed. Finally, we examined whether 2ME accelerates oviductal egg transport in unmated rats that were previously treated with a rat recombinant TNF-α alone or concomitant with a selective inhibitor of the NFκB activity. Mating increased TNF-α in the oviductal fluid, but Tnfa transcript was not detected in the oviduct. The mRNA for TNF-α receptors as well as their distribution was not affected by mating although they were mainly localized in the endosalpinx. Administration of TNF-α into the oviduct of unmated rats prevented the effect of 2ME on egg transport. However, the NF-κB activity inhibitor did not revert this effect of TNF-α. These results indicate that mating increased TNF-α in the oviductal fluid, although this not associated with changes in the expression and localization of TNF-α receptors in the oviductal cells. Furthermore, TNF-α mimicked the effect of mating on the 2ME-induced egg transport acceleration, independently of the activation of NFκB in the oviduct. We concluded that TNF-α is the signal induced by mating to shut down a 2ME nongenomic action in the rat oviduct.
Reproduction 11/2012; · 2.58 Impact Factor
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ABSTRACT: BACKGROUND: One of the unique characteristics of the female genital tract is the extensive tissue remodeling observed throughout the menstrual cycle. Multiple components of the extracellular matrix take part in this tissue rebuilding; however, the individual components involved have not been identified. METHODS: In the present study, the expression of extracellular matrix proteins and selected matrix metalloproteinase (MMP) activities in Fallopian tubes (FT) throughout the menstrual cycle were examined by PCR array, immunocytochemistry, zymography and bioinformatics. RESULTS: Of the eighty-four genes analyzed, eighty-three were expressed in the FT during at least one stage of the menstrual cycle. We observed a significant increase (>/=2-fold) in ADAMTS1, ADAMTS13, COL7A1, MMP3, MMP9, PECAM1, and THBS3 in the periovulatory phase compared to the follicular phase. Meanwhile, we observed a significant decrease (>/= 2-fold) in COL7A1, ICAM1, ITGA8, MMP16, MMP9, CLEC3B, SELE and TIMP2 in the lutheal phase compared to the periovulatory phase. Immunocytochemistry showed that MMP-3 and MMP-9 were localized in the endosalpinx during all phases of the menstrual cycle. Gelatin zymograms detected non-cycle-dependent protease activity. CONCLUSIONS: Several extracellular matrix components were regulated throughout the menstrual cycle in a cyclic pattern, suggesting a possible steroid regulation and a role in tissue remodeling and FT functions.
Reproductive Biology and Endocrinology 08/2012; 10(1):56. · 2.05 Impact Factor
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ABSTRACT: A role for pilus during attachment of Neisseria gonorrhoeae to epithelia of the female reproductive tract is currently assumed. However, Pil⁻ gonococci have been observed during infection of the reproductive tract, which prompted us to examine the effect of pili on the dynamics of infection and the inflammatory responses of mucosal explants of the human fallopian tube.
Mucosal explants were infected in vitro with Opa negative Pil⁻ and Pil⁺N. gonorrhoeae strains.
Piliation enhanced gonococcal adherence to the epithelium within 3 h of infection (P < 0.05) but thereafter did not offer advantage to gonococci to colonize the epithelial cell surface (P > 0.05). No differences were found between the strains in numbers of gonococci inside epithelial cells. Pil⁻ bacteria induced higher levels (P < 0.05) of IL-1β, TNF-α, GM-CSF, MCP-1, and MIP-1β than Pil⁺ bacteria. There were no differences between both strains in LOS pattern, and Pil expression did not change after coincubation with mucosal strips.
Results show that gonococcal invasion of the human fallopian tube can occur independently of pilus or Opa expression, and suggest that pilus, by inhibition of several key elements of the initial inflammatory response, facilitates sustained infection of this organ.
Journal of Biomedicine and Biotechnology 01/2012; 2012:491298. · 2.44 Impact Factor
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ABSTRACT: To compare mRNA and protein levels of proenkephalin A (PEA) and gamma-aminobutyric acid A receptor pi subunit (piGABA-R) in human secretory endometrium before and during receptivity and to determine the cell phenotypes where they are expressed.
Prospective and observational, comparing prereceptive vs. receptive stages of secretory endometrium within the same nonconceptional menstrual cycle.
University and non-governmental organization (NGO)-based academic and clinical-research facilities.
Seven healthy, multiparous, surgically sterilized women with spontaneous regular menstrual cycles.
Endometrial biopsies were obtained on LH+3 and LH+7 within the same cycle.
Levels of PEA and piGABA-R mRNA were determined by real-time PCR, and protein presence, by immunofluorescence.
The mRNA level of PEA fell, whereas that of piGABA-R increased, during endometrial receptivity. Positive immunostaining of PEA was found in the luminal and glandular epithelium, whereas that of piGABA-R was in luminal epithelium and stromal cells.
The discrete cell-phenotype localization and timing of the changes in the level of PEA and of piGABA-R mRNA and protein suggest an important role for these molecules in switching the human endometrium from a refractory to a receptive state.
Fertility and sterility 01/2007; 86(6):1750-7. · 3.97 Impact Factor
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Priscilla Morales,
Paz Reyes,
Macarena Vargas,
Miguel Rios,
Mónica Imarai, Hugo Cardenas,
Horacio Croxatto,
Pedro Orihuela,
Renato Vargas,
Juan Fuhrer,
John E Heckels,
Myron Christodoulides,
Luis Velasquez
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ABSTRACT: Following infection with Neisseria gonorrhoeae, bacteria may ascend into the Fallopian tubes (FT) and induce salpingitis, a major cause of infertility. In the FT, interactions between mucosal epithelial cells and gonococci are pivotal events in the pathogen's infection cycle and the inflammatory response. In the current study, primary FT epithelial cells were infected in vitro with different multiplicities of infection (MOI) of Pil+ Opa+ gonococci. Bacteria showed a dose-dependent association with cells and induced the secretion of tumor necrosis factor alpha (TNF-alpha). A significant finding was that gonococcal infection (MOI = 1) induced apoptosis in approximately 30% of cells, whereas increasing numbers of bacteria (MOI = 10 to 100) did not induce apoptosis. Apoptosis was observed in only 11% of cells with associated bacteria, whereas >84% of cells with no adherent bacteria were apoptotic. TNF-alpha was a key contributor to apoptosis, since (i) culture supernatants from cells infected with gonococci (MOI = 1) induced apoptosis in naïve cultures, suggesting that a soluble factor was responsible; (ii) gonococcal infection-induced apoptosis was inhibited with anti-TNF-alpha antibodies; and (iii) the addition of exogenous TNF-alpha induced apoptosis, which was inhibited by the presence of increasing numbers of bacteria (MOI = 10 to 100). These data suggest that TNF-alpha-mediated apoptosis of FT epithelial cells is likely a primary host defense mechanism to prevent pathogen colonization. However, epithelial cell-associated gonococci have evolved a mechanism to protect the cells from undergoing TNF-alpha-mediated apoptosis, and this modulation of the host innate response may contribute to establishment of infection. Understanding the antiapoptotic mechanisms used by Neisseria gonorrhoeae will inform the pathogenesis of salpingitis and could suggest new intervention strategies for prevention and treatment of the disease.
Infection and Immunity 06/2006; 74(6):3643-50. · 4.16 Impact Factor
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ABSTRACT: Infection of the Fallopian tubes (FT) by Neisseria gonorrhoeae can lead to acute salpingitis, an inflammatory condition, which is a major cause of infertility. Challenge of explants of human FT with gonococci induced mRNA expression and protein secretion for the proinflammatory cytokines interleukin (IL)-1alpha, IL-1beta, and tumor necrosis factor alpha (TNF-alpha) but not for granulocyte-macrophage colony-stimulating factor. In contrast, FT expression of IL-6 and of the cytokine receptors IL-6R, TNF receptor I (TNF-RI), and TNF-RII was constitutive and was not increased by gonococcal challenge. These studies suggest that several proinflammatory cytokines are likely to contribute to the cell and tissue damage observed in gonococcal salpingitis.
Infection and Immunity 02/2003; 71(1):527-32. · 4.16 Impact Factor
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Fertility and Sterility 04/2002; 77(3):633-4. · 3.56 Impact Factor
