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      Histamine and TNF-α release by rat peritoneal mast cells stimulated with Trichomonas vaginalis Translated title: Histamine et TNF-α secrétés par les mastocytes péritonéaux stimulés par Trichomonas vaginalis chez le rat

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          Abstract

          Mast cells have been reported to be predominant in the vaginal smears of patients infected with T. vaginalis. In this study, we investigated whether T. vaginalis could induce mast cells to migrate and to produce TNF-α and histamine. Rat peritoneal mast cells (RPMC), a primary mast cell, were used for the study. T. vaginalis induced an increase in chemotactic migration of the mast cells toward excretory and secretory product (ESP) of T. vaginalis, and the mast cells activated with T. vaginalis showed an increased release of histamine and TNF-α. Therefore, mast cells may be involved in the inflammatory response caused by T. vaginalis.

          Translated abstract

          Les mastocytes sont observés en quantité importante dans les sécrétions vaginales de patientes infectées par T. vaginalis. Cette étude explore pourquoi T. vaginalis induit la migration des mastocytes et leur production de TNF-α et d’histamine. Des mastocytes péritonéaux du rat ont été utilisés pour cette étude. Les produits d’excrétion-sécrétion de T. vaginalis induisent une augmentation de la migration chémotactique des mastocytes, et les mastocytes ainsi activés par T. vaginalis augmentent leur production d’histamine et de TNF-α. Les mastocytes seraient donc impliqués dans la réaction inflammatoire à T. vaginalis.

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          Most cited references 27

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          Mast cell modulation of neutrophil influx and bacterial clearance at sites of infection through TNF-alpha.

          Although mast cells have been implicated in a variety of inflammatory conditions including immediate hypersensitivity and interstitial cystitis, their physiological role in the body is unknown. We investigated the role of mast cells in host defence against bacterial infections using a well characterized mast-cell-deficiency mouse model. We report here that mast cells, which are selectively located at portals of bacterial entry, are important to host defence. Mast-cell-deficient WBB6F1-W/Wv mice (W/Wv) were up to 20-fold less efficient in clearing enterobacteria than control WBB6F1 +/+ (+/+) mice or mast-cell-reconstituted W/Wv (W/Wv+MC) mice. With higher bacteria inocula, only W/Wv mice died (80%). The limited bacterial clearance in W/Wv mice directly correlated with impaired neutrophil influx. The mast-cell chemoattractant TNF-alpha was implicated in the neutrophil response because TNF-alpha was locally released only in +/+ and W/Wv+MC mice, TNF-alpha-specific antibodies blocked over 70% of the neutrophil influx, and purified mast cells released TNF-alpha upon incubation with bacteria. Additionally, the type-1 fimbrial subunit, FimH, was the necessary enterobacterial component for mast-cell activation and neutrophil influx because an isogenic FimH- mutant evoked a limited neutrophil response in +/+ mice compared to wild-type bacteria.
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            Trichomonas vaginalis associated with low birth weight and preterm delivery. The Vaginal Infections and Prematurity Study Group.

            Several studies have suggested that pregnant women infected with Trichomonas vaginalis may be at increased risk of an adverse outcome. To evaluate prospectively the association between T. vaginalis and risk of adverse pregnancy outcome in a large cohort of ethnically diverse women. At University-affiliated hospitals and antepartum clinics in five United States cities, 13,816 women (5,241 black, 4,226 Hispanic, and 4,349 white women) were enrolled at mid-gestation, tested for T. vaginalis by culture, and followed up until delivery. The prevalence of T. vaginalis infection at enrollment was 12.6%. Race-specific prevalence rates were 22.8% for black, 6.6% for Hispanic, and 6.1% for white women. After multivariate analysis, vaginal infection with T. vaginalis at mid-gestation was significantly associated with low birth weight (odds ratio 1.3; 95% confidence interval 1.1 to 1.5), preterm delivery (odds ratio 1.3; 95% confidence interval 1.1 to 1.4), and preterm delivery of a low birth weight infant (odds ratio 1.4; 95% confidence interval 1.1 to 1.6). The attributable risk of T. vaginalis infection associated with low birth weight weight in blacks was 11% compared with 1.6% in Hispanics and 1.5% in whites. After considering other recognized risk factors including co-infections, pregnant women infected with T. vaginalis at mid-gestation were statistically significantly more likely to have a low birth weight infant, to deliver preterm, and to have a preterm low birth weight infant. Compared with whites and Hispanics, T. vaginalis infection accounts for a disproportionately larger share of the low birth weight rate in blacks.
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              Mast Cells Control Neutrophil Recruitment during T Cell–Mediated Delayed-Type Hypersensitivity Reactions through Tumor Necrosis Factor and Macrophage Inflammatory Protein 2

              Polymorphonuclear leukocytes (PMNs) characterize the pathology of T cell–mediated autoimmune diseases and delayed-type hypersensitivity reactions (DTHRs) in the skin, joints, and gut, but are absent in T cell–mediated autoimmune diseases of the brain or pancreas. All of these reactions are mediated by interferon γ–producing type 1 T cells and produce a similar pattern of cytokines. Thus, the cells and mediators responsible for the PMN recruitment into skin, joints, or gut during DTHRs remain unknown. Analyzing hapten-induced DTHRs of the skin, we found that mast cells determine the T cell–dependent PMN recruitment through two mediators, tumor necrosis factor (TNF) and the CXC chemokine macrophage inflammatory protein 2 (MIP-2), the functional analogue of human interleukin 8. Extractable MIP-2 protein was abundant during DTHRs in and around mast cells of wild-type (WT) mice but absent in mast cell–deficient WBB6F1-KitW /KitW- v (KitW /KitW -v) mice. T cell–dependent PMN recruitment was reduced >60% by anti–MIP-2 antibodies and >80% in mast cell–deficient KitW /KitW -v mice. Mast cells from WT mice efficiently restored DTHRs and MIP-2–dependent PMN recruitment in KitW /KitW -v mice, whereas mast cells from TNF−/− mice did not. Thus, mast cell–derived TNF and MIP-2 ultimately determine the pattern of infiltrating cells during T cell–mediated DTHRs.
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                Author and article information

                Journal
                Parasite
                Parasite
                parasite
                Parasite : journal de la Société Française de Parasitologie
                EDP Sciences
                1252-607X
                1776-1042
                February 2011
                15 February 2011
                : 18
                : 1 ( publisher-idID: parasite/2011/01 )
                : 49-55
                Affiliations
                [1 ] Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine #17 Haengdang-dong Sungdong-gu, Seoul 133-791 Korea
                [2 ] Department of Parasitology, School of Medicine, Catholic University of Daegu Daegu 705-718 Korea
                [3 ] Department of Biochemistry and Molecular Biology, Hanyang University College of Medicine Seoul 133-791 Korea
                [4 ] Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University Seoul 130-701 Korea
                Author notes
                [* ]Correspondence: Jae-Sook Ryu. Tel.: 82 2 2220 0683 – Fax: 82 2 2281 6519. E-mail: jsryu@ 123456hanyang.ac.kr

                N.B.: Im S.J. and Ahn M.H. contributed equally to this work.

                Article
                parasite2011181p49 10.1051/parasite/2011181049
                10.1051/parasite/2011181049
                3671398
                21395205
                © PRINCEPS Editions, Paris, 2011

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 39, Pages: 7
                Categories
                Original Contribution

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