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Antifungal Activities of a Pasture Honey and Ginger (Ziginber Officinale) Extracts on Some Pathogenic Fungi
FO Omoya
Journal of Science and Technology (Ghana) , 2012,
Abstract: Methanol, ethanol, ginger extracts and a pasture honey were tested on Aspergillus flavus, Aspergillus fumigatus, Trichoderma viride and Candida albicans using the well-in-agar method. The antifungal sensitivity assay indicated that the chemical solvent extracts of ginger, pasture honey and mixtures of honey and ginger extracts exerted inhibitory zones on the test fungi species except A. Fumigatus. However, the pasture honey displayed higher inhibitory values of 45 mm than the mixtures of honey and ethanol extract of ginger and honey and methanol extract of ginger with 40 mm and 30 mm inhibitory zones respectively. The phytochemicals present in honey were saponin and cardiac glycoside, while in the ginger sample, saponin, phlobatannin, alkaloids, flavonoids and cardiac glycoside were present. Summarily, honey and ginger extracts displayed the highest inhibitory activity on all the tested fungal isolates compared to the employed positive control antifungal (Griseofulvin and Ketoconazole).
Mixture of honey and ginger extract for antibacterial assessment on some clinical isolates.  [PDF]
International Journal of Pharmaceutical and Biological Research , 2011,
Abstract: The antibacterial activity of honey, methanol and ethanol extracts of ginger (Zingiber officinale) were investigated against some selected bacteria using the agar diffusion technique. Two Gram positive and four Gram negative bacteria were assessed for possible inhibition by the extract samples. The inhibitory potency of the extracts on the test organisms varied in the halos as inhibition effects. Though all the test organisms were susceptible to the antibacterial samples with inhibition measure between 6-3mm, E. coli was the most inhibited where an inhibitory measure of 20mm was recorded with honey, 18mm with ginger ethanol extract and 32mm with the mixture of honey and ginger ethanol extract. The pasture honey, the ethanol and methanol extracts of ginger were both positive for saponin and cardiac glycosides among the phytochemicals identified. While some of the commercial antibiotics (positive control) were not effective on the test organisms, gentamycin and streptomycin were effective with inhibitory halos ranging between 8-25mm. However, the antibacterial test samples were higher in inhibition values than the reference drugs (positive control).
Combine Antimicrobial Effect of Ginger and Honey on Some Human Pathogens  [cached]
O. Yahaya,J.A.Yabefa,I.O. Umar,M. Datshen
British Journal of Pharmacology and Toxicology , 2012,
Abstract: The aim of this study is to determine the antibacterial effects of different honey samples on clinically isolated bacteria species. Ginger (Zingiber officinales) and honey are one of the nature gifts to mankind and have been used to prevent and control disease conditions. The crude extracts of the plant materials were used with pure honey collected from various parts of Kogi State. The Agar diffusion method was used to determine the antimicrobial activity of the plant extracts, honey and combination of both against Salmonella typhi, Shigella dysenteriae, Escherichia coli and Candida albican. The growth of all test organisms were inhibited though to varying degrees by the plant extract and honey and with greater effect when combined thus justifying their use in traditional medicines in treating enteric infection and other diseases across Africa.
Inhibition of Aldose Reductase Prevents Experimental Allergic Airway Inflammation in Mice  [PDF]
Umesh C. S. Yadav, Kota V. Ramana, Leopoldo Aguilera-Aguirre, Istvan Boldogh, Hamid A. Boulares, Satish K. Srivastava
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006535
Abstract: Background The bronchial asthma, a clinical complication of persistent inflammation of the airway and subsequent airway hyper-responsiveness, is a leading cause of morbidity and mortality in critically ill patients. Several studies have shown that oxidative stress plays a key role in initiation as well as amplification of inflammation in airways. However, still there are no good anti-oxidant strategies available for therapeutic intervention in asthma pathogenesis. Most recent studies suggest that polyol pathway enzyme, aldose reductase (AR), contributes to the pathogenesis of oxidative stress–induced inflammation by affecting the NF-κB-dependent expression of cytokines and chemokines and therefore inhibitors of AR could be anti-inflammatory. Since inhibitors of AR have already gone through phase-III clinical studies for diabetic complications and found to be safe, our hypothesis is that AR inhibitors could be novel therapeutic drugs for the prevention and treatment of asthma. Hence, we investigated the efficacy of AR inhibition in the prevention of allergic responses to a common natural airborne allergen, ragweed pollen that leads to airway inflammation and hyper-responsiveness in a murine model of asthma. Methods and Findings Primary Human Small Airway Epithelial Cells (SAEC) were used to investigate the in vitro effects of AR inhibition on ragweed pollen extract (RWE)-induced cytotoxic and inflammatory signals. Our results indicate that inhibition of AR prevents RWE -induced apoptotic cell death as measured by annexin-v staining, increase in the activation of NF-κB and expression of inflammatory markers such as inducible nitric oxide synthase (iNOS), cycloxygenase (COX)-2, Prostaglandin (PG) E2, IL-6 and IL-8. Further, BALB/c mice were sensitized with endotoxin-free RWE in the absence and presence of AR inhibitor and followed by evaluation of perivascular and peribronchial inflammation, mucin production, eosinophils infiltration and airway hyperresponsiveness. Our results indicate that inhibition of AR prevents airway inflammation and production of inflammatory cytokines, accumulation of eosinophils in airways and sub-epithelial regions, mucin production in the bronchoalveolar lavage fluid and airway hyperresponsiveness in mice. Conclusions These results suggest that airway inflammation due to allergic response to RWE, which subsequently activates oxidative stress-induced expression of inflammatory cytokines via NF-κB-dependent mechanism, could be prevented by AR inhibitors. Therefore, inhibition of AR could have clinical implications, especially for
GITR signaling potentiates airway hyperresponsiveness by enhancing Th2 cell activity in a mouse model of asthma
Alexandre C Motta, Joost LM Vissers, Renée Gras, Betty CAM Van Esch, Antoon JM Van Oosterhout, Martijn C Nawijn
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-93
Abstract: CD4+CD25- cells were polarized in vitro into Th1 and Th2 effector cells, and re-stimulated in the presence of GITR agonistic antibodies to assess the effect on IFNγ and IL-4 production. To evaluate the effects of GITR stimulation on AHR and allergic inflammation in a mouse asthma model, BALB/c mice were sensitized to OVA followed by airway challenges in the presence or absence of GITR agonist antibodies.GITR engagement potentiated cytokine release from CD3/CD28-stimulated Th2 but not Th1 cells in vitro. In the mouse asthma model, GITR triggering at the time of challenge induced enhanced airway hyperresponsiveness, serum IgE and ex vivo Th2 cytokine release, but did not increase BAL eosinophilia.GITR exerts a differential effect on cytokine release of fully differentiated Th1 and Th2 cells in vitro, potentiating Th2 but not Th1 cytokine production. This effect on Th2 effector functions was also observed in vivo in our mouse model of asthma, resulting in enhanced AHR, serum IgE responses and Th2 cytokine production. This is the first report showing the effects of GITR activation on cytokine production by polarized primary Th1 and Th2 populations and the relevance of this pathway for AHR in mouse models for asthma. Our data provides crucial information on the mode of action of the GITR signaling, a pathway which is currently being considered for therapeutic intervention.Allergic asthma is an inflammatory disease characterized by reversible airway obstruction, and is associated with airways hyperresponsiveness (AHR) to bronchospasmogenic compounds, elevated allergen-specific IgE serum levels and chronic airway eosinophilia [1]. Th2 cells are known to be critical for the induction of allergic asthma manifestations by the production of IL-4, IL-5 and IL-13. Regulatory T (Treg) cells can counteract Th2 cell activity, and have the ability to suppress AHR and allergic inflammation upon allergen provocation in mouse models of allergic asthma. For instance, adoptive transfer o
Maintenance of Airway Hyperresponsiveness in Chronic Asthma May Be Mediated by Th2-Independent Mechanisms
Nora J. Lin, Jane M. SchuhCory HogaboamAspergillus fumigatusA. fumigatus
The Open Allergy Journal , 2008, DOI: 10.2174/1874838400801010012]
Abstract: ICD4+, Th2-mediated inflammation is an important component of airway hyperresponsiveness (AHR) in allergic airway disease. IL-4 specifically interacts with the Type 1 IL-4 receptor comprised of IL-4Rα and the common γ chain, whereas IL-4 and IL-13 mediate their effects through a common receptor complex made up of IL-4Rα and IL- 13Rα1 (i.e. the Type II IL-4 receptor). In this study, we examined the effects of impaired Th2 signaling on AHR using IL4Rα-/- mice in a murine model of allergic asthma. IL-4Rα-/- mice and control BALB/c (IL-4Rα+/+) mice were sensitized to and challenged with Aspergillus fumigatus. Airway disease was assessed at days 14, 28, 51, and 57 after intratracheal conidia challenge. AHR was evaluated by plethysmography after intravenous methacholine. Whole lung levels of cytokines and chemokines, and serum immunoglobulins were measured by specific ELISA. Paraffin-embedded lung sections were stained for histology. Bronchoalveolar lavage (BAL) fluid was cytospun for differential cell counts. While AHR was significantly reduced in IL-4Rα-/- mice (p<0.01) at days 14 and 28 after conidia challenge, it was increased when compared to controls at later time points (days 51 and 57) even though Th2 cytokines were significantly decreased at day 57, and total IgE and IgG1 levels were markedly decreased throughout the study (p<0.0001). Goblet cell metaplasia was also evident at days 51 and 57 in the knockout groups. These results demonstrate that airway hyperresponsiveness and mucus cell metaplasia in a model of allergic asthma can develop in the absence of a predominant Th2 signaling pathway, suggesting that Th2-independent mechanisms may arbitrate chronic stages of airway disease due to A. fumigatus.
Honey prevents hepatic damage induced by obstruction of the common bile duct  [cached]
B Imge Erguder, Sibel S Kilicoglu, Mehmet Namuslu, Bulent Kilicoglu, Erdinc Devrim, Kemal Kismet, Ilker Durak
World Journal of Gastroenterology , 2008,
Abstract: AIM: To examine the possible effects of honey supplementation on hepatic damage due to obstruction of the common bile duct in an experimental rat model.METHODS: The study was performed with 30 male rats divided into three groups: a sham group, an obstructive jaundice group, and an obstructive jaundice plus honey group. At the end of the study period, the animals were sacrificed, and levels of nitric oxide (NO), and NO synthase (NOS) activities were measured in liver tissues, and levels of adenosine deaminase (ADA) and alanine transaminase (ALT) activities were measured in serum.RESULTS: Blood ALT and ADA activities were significantly elevated in the jaundice group as compared to those of the sham group. In the obstructive jaundice plus honey group, blood ALT and ADA activities were significantly decreased as compared to those of the jaundice group. In erythrocytes and liver tissues, NO levels were found to be significantly higher in the obstructive jaundice plus honey group compared to those of the sham group. Additionally, NO levels were found to be significantly higher in liver tissues from the animals in the obstructive jaundice plus honey group than those of the jaundice group.CONCLUSION: Honey was found to be beneficial in the prevention of hepatic damage due to obstruction of the common bile duct.
The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation  [PDF]
Jesse W. Williams,Melissa Y. Tjota,Anne I. Sperling
Journal of Allergy , 2012, DOI: 10.1155/2012/236075
Abstract: In both human asthmatics and animal models of allergy, allergen-specific IgG can contribute to Th2-mediated allergic inflammation. Mouse models have elucidated an important role for IgG and Fc-gamma receptor (FcγR) signaling on antigen presenting cells (APC) for the induction of airway inflammation. These studies suggest a positive feedback loop between IgG produced by the adaptive B cell response and FcγR signaling on innate immune cells. Studies of IgG and FcγRs in humans with asthma or allergic lung disease have been more controversial. Some reports have identified associations between allergen-specific IgG and severity of allergic responses, while other studies have found associations of IgG subclass IgG4 with allergic tolerance. In this paper, we review the literature to help define the nature of IgG and FcγR signaling on innate immune cells and how it contributes to the development of allergic immune responses. 1. Atopic Asthma Is Commonly Associated with Th2 Responses Asthma is a chronic inflammatory disease of the lungs marked by recurrent episodes of airway hyperresponsiveness resulting in chest tightness, wheezing, and shortness of breath. Allergic or atopic asthma is the most common form of asthma, and allergic sensitization occurs in about 80% of asthmatic children and 60% of asthmatic adults [1]. Although there are now multiple phenotypes for atopic asthma, it has been classically associated with an excessive Th2-driven inflammatory response [2]. Development of an aberrant Th2 response leads to production of several cytokines including IL-4, IL-5, IL-9, and IL-13 that results in eosinophilia, goblet cell hyperplasia, mast cells activation, and smooth muscle hypertrophy [3]. In addition to these cellular effects, there is an important humoral response generated during primary sensitization that leads to production of allergen-specific IgE and IgG1. Much of the interest in dissecting the pathogenesis of asthma has focused on allergen-specific IgE which is well known to induce allergic hypersensitivity [4]. However, it was found that IgE?/? mice were still able to develop anaphylaxis and airway hyperreactivity suggesting that other mediators including allergen-specific IgG could be playing an important role in disease pathogenesis [5, 6]. Moreover, the total allergen-specific IgG response is greater in magnitude and has a significantly increased half-life compared to the total allergen-specific IgE response [7]. The complex nature of IgE in promoting allergy can be reviewed in a variety of recent articles [8–10]. In this review, we discuss
Aldose Reductase Inhibition Prevents Metaplasia of Airway Epithelial Cells  [PDF]
Umesh C. S. Yadav,Leopoldo Aguilera-Aguirre,Kota V. Ramana,Istvan Boldogh,Satish K. Srivastava
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0014440
Abstract: Goblet cell metaplasia that causes mucus hypersecretion and obstruction in the airway lumen could be life threatening in asthma and chronic obstructive pulmonary disease patients. Inflammatory cytokines such as IL-13 mediate the transformation of airway ciliary epithelial cells to mucin-secreting goblet cells in acute as well as chronic airway inflammatory diseases. However, no effective and specific pharmacologic treatment is currently available. Here, we investigated the mechanisms by which aldose reductase (AR) regulates the mucus cell metaplasia in vitro and in vivo.
Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2
Laura L Koth, Madeleine W Rodriguez, Xin Bernstein, Salina Chan, Xiaozhu Huang, Israel F Charo, Barrett J Rollins, David J Erle
Respiratory Research , 2004, DOI: 10.1186/1465-9921-5-12
Abstract: To test whether MCP-1 and CCR2 are each required for the development of experimental allergic asthma, we applied an Aspergillus antigen-induced model of Th2 cytokine-driven allergic asthma associated with airway fibrosis to mice deficient in either MCP-1 or CCR2. Previous studies with live Aspergillus conidia instilled into the lung revealed that MCP-1 and CCR2 play a role in anti-fungal responses; in contrast, we used a non-viable Aspergillus antigen preparation known to induce a robust eosinophilic inflammatory response.We found that wild-type C57BL/6 mice developed eosinophilic airway inflammation, goblet cell hyperplasia, airway hyperreactivity, elevations in serum IgE, and airway fibrosis in response to airway challenge with Aspergillus antigen. Surprisingly, mice deficient in either MCP-1 or CCR2 had responses to Aspergillus antigen similar to those seen in wild-type mice, including production of Th2 cytokines.We conclude that robust Th2-mediated lung pathology can occur even in the complete absence of MCP-1 or CCR2.Monocyte chemoattractant protein-1 (MCP-1, also known as CCL2) and its receptor, CCR2, have been the focus of intense interest due to increasing awareness of their association with debilitating human diseases, including asthma [1-3] and pulmonary fibrosis [4-7]. Since MCP-1 attracts and activates a variety of cells, including monocytes, immature dendritic cells, basophils, natural killer cells, and a subset of T lymphocytes [8-17], MCP-1 may have multiple roles in the immune response. Models of Th1 or Th2 inflammation applied to mice deficient in either MCP-1 or CCR2 have clearly shown important roles for this chemokine and its receptor in the development of inflammation [18-24]. However, results obtained using allergen-induced models of asthma (ovalbumin and cockroach antigen) in CCR2-deficient mice are varied, showing either increased, decreased or unchanged Th2 inflammation and airway hyperreactivity (AHR) [25-27], possibly due to differences in

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