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      Ginger and Cinnamon: Can This Household Remedy Treat Giardiasis? Parasitological and Histopathological Studies

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          Abstract

          Background

          Giardia lamblia is one of the most common protozoal infections in human especially children. Metronidazol (MTZ) is the drug of choice for treatment of giardiasis; its chemical composition possesses major threats and is becoming less sensitive. This study aimed to search for natural extracts alternative to MTZ.

          Methods

          In-vivo effects of dichloromethane extracts of ginger and cinnamon in doses of 10 and 20 mg/kg/day separately were studied on 30 experimentally infected albino rats divided into 6 groups (5 rats each). Plant extracts were started on the 6th day post infection for 7 successive days. The study was evaluated by fecal cyst and intestinal trophozoite counts, histopathology, scanning and transmission electron microscopic examinations of the small intestinal mucosa.

          Results

          Ginger and cinnamon caused reduction of fecal cyst and trophozoites counts. Histopathology, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) after exposure to each extract revealed evident improvement of intestinal mucosal damage produced by G. lamblia infection and direct structural injury to the trophozoites. However, these results were more obvious after exposure to cinnamon extracts.

          Conclusion

          We confirmed the potential therapeutic effects of ginger and cinnamon extracts on G. lamblia infection in albino rats as a promising alternative therapy to the commonly used antigiardial drugs.

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          Most cited references59

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          Intestinal Goblet Cells and Mucins in Health and Disease: Recent Insights and Progress

          The mucus layer coating the gastrointestinal tract is the front line of innate host defense, largely because of the secretory products of intestinal goblet cells. Goblet cells synthesize secretory mucin glycoproteins (MUC2) and bioactive molecules such as epithelial membrane-bound mucins (MUC1, MUC3, MUC17), trefoil factor peptides (TFF), resistin-like molecule β (RELMβ), and Fc-γ binding protein (Fcgbp). The MUC2 mucin protein forms trimers by disulfide bonding in cysteine-rich amino terminal von Willebrand factor (vWF) domains, coupled with crosslinking provided by TFF and Fcgbp proteins with MUC2 vWF domains, resulting in a highly viscous extracellular layer. Colonization by commensal intestinal microbiota is limited to an outer “loose” mucus layer, and interacts with the diverse oligosaccharides of mucin glycoproteins, whereas an “inner” adherent mucus layer is largely devoid of bacteria. Defective mucus layers resulting from lack of MUC2 mucin, mutated Muc2 mucin vWF domains, or from deletion of core mucin glycosyltransferase enzymes in mice result in increased bacterial adhesion to the surface epithelium, increased intestinal permeability, and enhanced susceptibility to colitis caused by dextran sodium sulfate. Changes in mucin gene expression and mucin glycan structures occur in cancers of the intestine, contributing to diverse biologic properties involved in the development and progression of cancer. Further research is needed on identification and functional significance of various components of mucus layers and the complex interactions among mucus layers, microbiota, epithelial cells, and the underlying innate and adaptive immunity. Further elucidation of the regulatory mechanisms involved in mucin changes in cancer and inflammation may lead to the development of novel therapeutic approaches.
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            Effect of chronic Giardia lamblia infection on epithelial transport and barrier function in human duodenum.

            Giardia lamblia causes infection of the small intestine, which leads to malabsorption and chronic diarrhoea. To characterise the inherent pathomechanisms of G lamblia infection. Duodenal biopsy specimens from 13 patients with chronic giardiasis and from controls were obtained endoscopically. Short-circuit current (I(SC)) and mannitol fluxes were measured in miniaturised Ussing chambers. Epithelial and subepithelial resistances were determined by impedance spectroscopy. Mucosal morphometry was performed and tight junction proteins were characterised by immunoblotting. Apoptotic ratio was determined by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling staining. In giardiasis, mucosal surface area per unit serosa area was decreased to 75% (3%) of control, as a result of which epithelial resistance should increase. Instead, epithelial resistance of giardiasis biopsy specimens was decreased (19 (2) vs 25 (2) Omega cm(2); p<0.05) whereas mannitol flux was not significantly altered (140 (27) vs 105 (16) nmol/h/cm(2)). As structural correlate, reduced claudin 1 expression and increased epithelial apoptosis were detected. Furthermore, basal I(SC) increased from 191 (20) in control to 261 (12) microA/h/cm(2) in giardiasis. The bumetanide-sensitive portion of I(SC) in giardiasis was also increased (51 (5) vs 20 (9) microA/h/cm(2) in control; p<0.05). Finally, phlorizin-sensitive Na(+)-glucose symport was reduced in patients with giardiasis (121 (9) vs 83 (14) microA/h/cm(2)). G lamblia infection causes epithelial barrier dysfunction owing to down regulation of the tight junction protein claudin 1 and increased epithelial apoptoses. Na(+)-dependent d-glucose absorption is impaired and active electrogenic anion secretion is activated. Thus, the mechanisms of diarrhoea in human chronic giardiasis comprise leak flux, malabsorptive and secretory components.
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              Strain-dependent induction of enterocyte apoptosis by Giardia lamblia disrupts epithelial barrier function in a caspase-3-dependent manner.

              We recently demonstrated that Giardia lamblia rearranges cytoskeletal proteins and reduces transepithelial electrical resistance. The effect of G. lamblia on enterocyte apoptosis is unknown, and a possible link between microbially induced enterocyte apoptosis and altered epithelial permeability has yet to be established. The aim of this study was to assess whether G. lamblia induces enterocyte apoptosis in duodenal epithelial monolayers and whether this effect increases epithelial permeability. Monolayers of nontransformed human duodenal epithelial cells were incubated with sonicated or live G. lamblia trophozoites (NF, S2, WB, or PB strains) for 8, 24, and 48 h. Cell cultures were assessed for apoptosis by Hoechst fluorescence staining, enzyme-linked immunosorbent assay for apoptotic nucleosomes, and electron microscopy. In separate experiments, monolayers were pretreated with or without 120 microM caspase-3 inhibitor (Z-DEVD-FMK) for 1 h and were assessed for production of apoptotic nucleosomes, tight junctional integrity (with fluorescent ZO-1 staining followed by confocal laser microscopy), and transepithelial permeability for fluorescein isothiocyanate-dextran. G. lamblia strains NF and S2, but not strains WB or PB, induced enterocyte apoptosis within the monolayers, and this effect was inhibited by Z-DEVD-FMK pretreatment. Using the G. lamblia NF isolate, additional experiments investigated the possible link between enterocyte apoptosis and altered epithelial permeability. G. lamblia NF disrupted tight junctional ZO-1 and increased epithelial permeability, but these effects were also prevented by pretreatment with the caspase-3 inhibitor. These findings indicate that strain-dependent induction of enterocyte apoptosis may contribute to the pathogenesis of giardiasis. This effect is responsible for a loss of epithelial barrier function by disrupting tight junctional ZO-1 and increasing permeability in a caspase-3-dependent manner.
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                Author and article information

                Journal
                Iran J Parasitol
                Iran J Parasitol
                IJPA
                Iranian Journal of Parasitology
                Tehran University of Medical Sciences
                1735-7020
                2008-238X
                Oct-Dec 2014
                : 9
                : 4
                : 530-540
                Affiliations
                [1 ]Dept. of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt
                [2 ]Dept. of Histology, Faculty of Medicine, Assiut University, Assiut, Egypt
                [3 ]Dept. of Pharmacognosy, Faculty of Pharmacy, Assiut University, Assiut, Egypt
                Author notes
                [* ]Correspondence abeerwns@ 123456yahoo.com
                Article
                10.4081/mr.2011.e25
                4345092
                25759734
                fa9104d5-d87d-4efd-baca-261d308577b6
                Copyright: © Iranian Journal of Parasitology & Tehran University of Medical Sciences

                This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

                History
                : 22 May 2014
                : 05 September 2014
                Categories
                Medical Sciences

                Parasitology
                giardia,ginger,cinnamon,intestinal-histopathology,electron microscopy
                Parasitology
                giardia, ginger, cinnamon, intestinal-histopathology, electron microscopy

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