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IL-8 mRNA in human gingival epithelial cells (HGECs) is up-regulated by Fusobacterium nucleatum, and up-/down-regulated by Porphyromonas gingivalis in a complex interaction in the early stages (< or = 4 h) after infection. The mechanisms involved in this regulation in response to F. nucleatum and/or P. gingivalis infection, and identification of co-regulated cytokine genes, are the focus of this investigation. Heat, formalin or protease treatment of F. nucleatum cells attenuated the IL-8 mRNA up-regulation. NF-kappaB, mitogen-activated protein kinase (MAPK) p38 and MAPK kinase/extracellular signal-regulated kinase (MEK/ERK) pathways were involved in IL-8 mRNA induction by F. nucleatum. Pretreatment of P. gingivalis with heat, formalin or protease enhanced IL-8 mRNA induction. NF-kappaB, MARK p38, and MEK/ERK pathways were also involved in this induction. In contrast, down-regulation of IL-8 mRNA by P. gingivalis involved MEK/ERK, but not NF-kappaB or MAPK p38 pathways. cDNA arrays analysis revealed that mRNA down-regulation by P. gingivalis is a specific reaction that only a number of genes, e.g. IL-1beta, IL-8, macrophage inflammatory protein-2alpha, and migration inhibitory factor-related protein-14, are affected based on examination of 278 cytokine/receptor genes. These data indicate that F. nucleatum and P. gingivalis trigger specific and differential gene regulation pathways in HGECs. 相似文献
3.
Linda C. Lambert Hoa Q. Trummell Ashvani Singh Gail H. Cassell Robert J. Bridges 《Infection and immunity》1998,66(1):272-279
Murine chronic respiratory disease is characterized by persistent colonization of tracheal and bronchial epithelial cell surfaces by Mycoplasma pulmonis, submucosal and intraluminal immune and inflammatory cells, and altered airway activity. To determine the direct effect of M. pulmonis upon transepithelial ion transport in the absence of immune and inflammatory cell responses, primary mouse tracheal epithelial cell monolayers (MTEs) were apically infected and assayed in Ussing chambers. M. pulmonis-infected MTEs, but not those infected with a nonmurine mycoplasma, demonstrated reductions in amiloride-sensitive Na+ absorption, cyclic AMP, and cholinergic-stimulated Cl− secretion and transepithelial resistance. These effects were shown to require interaction of viable organisms with the apical surface of the monolayer and to be dependent upon organism number and duration of infection. Altered transport due to M. pulmonis was not merely a result of epithelial cell death as evidenced by the following: (i) active transport of Na+ and Cl−, albeit at reduced rates; (ii) normal cell morphology, including intact tight junctions, as demonstrated by electron microscopy; (iii) maintenance of a mean transepithelial resistance of 440 Ω/cm2; and (iv) lack of leakage of fluid from the basolateral to the apical surface of the monolayer. Alteration in epithelial ion transport in vitro is consistent with impaired pulmonary clearance and altered airway function in M. pulmonis-infected animals. Furthermore, the ability of M. pulmonis to alter transport without killing the host cell may explain its successful parasitism and long-term persistence in the host. Further study of the MTE-M. pulmonis model should elucidate the molecular mechanisms which mediate this reduction in transepithelial ion transport.Mycoplasmas, the smallest free-living prokaryotes, continue to be a significant cause of respiratory infections in a variety of animals, including humans (44). Their limited biosynthetic capability dictates that these organisms must both colonize and parasitize epithelial cell surfaces. It is therefore surprising that mycoplasmas produce diseases that are slowly progressing and chronic and yet often clinically inconspicuous. The molecular mechanisms responsible for this tenuous truce between the pathogen and the host cell have not yet been identified. Murine respiratory mycoplasmosis, a naturally occurring respiratory disease in laboratory rats and mice caused by Mycoplasma pulmonis (6, 8) and characterized by chronic, often lifelong tracheitis, bronchopneumonia, and bronchiectasis (7, 23, 28), would seem to be an ideal model with which to study these mechanisms. Although M. pulmonis-infected animals generate intense local and systemic immune responses (24, 33, 42, 43), they are incapable of eliminating the organism from the respiratory epithelium. Remodeling of the airways typically observed in infected animals, impairment of pulmonary clearance, and accumulation of mucus (23) suggest that M. pulmonis may compromise the ability of the epithelial cells to absorb and secrete fluid and electrolytes.Airway epithelial cells possess two major active transport processes, Na+ absorption and Cl− section. Water, in turn, osmotically follows the transepithelial movement of these ions, thereby providing a fluid film between the mucus layer and the epithelial cell surface. The depth and composition of this fluid microenvironment must be carefully regulated to allow the exchange of gases and the humidification of the airway epithelium and to ensure proper mucociliary clearance (47, 49). The consequences of impaired fluid and electrolyte transport in the airways are strikingly apparent in cases of cystic fibrosis, a recessive genetic disease resulting from the loss of epithelial chloride channels (31, 48). The studies reported here were designed to determine whether M. pulmonis infection alters electrolyte transport across the murine tracheal epithelium.The effect of bacteria upon mammalian epithelia in the absence of immune and inflammatory cells can be systematically evaluated by using the Ussing chamber model. Short-circuit current (Isc) studies have helped determine the mechanism by which cholera toxin (18) and other enterotoxins affect the intestinal mucosa (17, 35). Study of various types of epithelial cells by using the Ussing chamber model has also resulted in the identification of numerous microbial substances capable of directly altering the ion transport capacity of the airway epithelium (3, 20, 41).In the present study, control and M. pulmonis-infected mouse tracheal epithelial cells (MTEs) were evaluated in Ussing chambers. The results clearly show that M. pulmonis infection directly alters epithelial ion transport and that this alteration is species specific, dose and time related, and dependent upon the association of viable organisms with the apical cell surface. 相似文献
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Rabia Faridi Rizwan Yousaf Shoujun Gu Sayaka Inagaki Amy E. Turriff Keith Pelstring Bin Guan Amelia Naik Andrew J. Griffith Samuel Mawuli Adadey Elvis Twumasi Aboagye Gordon A. Awandare Robert J. Morell Ekaterini Tsilou Amanda G. Noyes Laura A. G. Sulmonte Ambroise Wonkam Isabelle Schrauwen Suzanne M. Leal Hela Azaiez Carmen C. Brewer Sheikh Riazuddin Robert B. Hufnagel Michael Hoa Wadih M. Zein J. Karl de Dios Thomas B. Friedman 《Clinical genetics》2023,103(6):699-703
6.
N. T. Kim Oanh B.-E. Bengtsson L. Bætz Reutergårdh D. T. Hoa P.-A. Bergqvist D. Broman Y. Zebühr 《Archives of environmental contamination and toxicology》1999,37(3):303-309
A bleached sulfate integrated pulp and paper mill producing printing and writing paper from mixed tropical hardwood and
bamboo was studied. The mill uses a “conventional bleaching sequence,” C-E-H1-H2, with an average molecular chlorine consumption
of 50 kg per ton of air-dried pulp (ADP). The content of polychlorinated dibenzofurans (PCDFs) and dibenzo-p-dioxins (PCDDs)
in the bleaching filtrate in terms of the nordic toxicity equivalent (N-TEQ) was 33.5, 1.15, 0.56, and 0.014 pg/L for the
E, C, H1, and H2 bleaching stages, respectively. The corresponding PCDFs and PCDDs loads in ng/t ADP were in the same ranking,
i.e., 670, 69, 11.2, and 0.28, respectively. The congener and isomeric pattern of PCDFs and PCDDs of the bleaching filtrate and
the bleached pulp was found to be typical for the chlorine bleaching plant effluent. The obtained dioxin load formed in the
mill is in agreement with Western studies for the given multiple chlorine of 0.21–0.23. The load is, however, lower than reported
discharges from Scandinavian mills using 1980s bleaching technologies, but substantially higher than the discharges from mills
with modern bleaching technologies. Modifications in the bleaching plant to reduce molecular chlorine use are necessary to
reduce dioxin formation.
Received: 15 July 1998/Accepted: 17 March 1999 相似文献
7.
J Robillard J E Couette J Le Mouel L Van Hoa J C Vernhes R Chédeville 《Journal de radiologie, d'électrologie, et de médecine nucléaire》1976,57(5):429-433
The purpose of the present work is to "quantify" bone scanning, in order to calculate indices of localized uptake that will make it possible to differentiate between normal and pathological uptake, and approach an etiologicial diagnosis. The authors use an Elscint dual head whole body scanner and an offline video display calculator. The patient is given 8 mc technetium 99m pyrophosphate 4 hours prior to scanning. The whole body count is expressed in thousands of counts multipled by two so that the knee to whole body ratio is close to one, to facilitate comparison of the indices. Results show that the presence of metastases is demonstrated more clearly by using a ratio bone segment to whole body. Quantitative scanning with 99mTc-pyrophosphate makes it possible to: 1) detect bone metastases easily, 2) follow the metastases during treatment, 3) avoid the gross errors that can be made in nomquantitative scanning. 相似文献
8.
Aruna Perera Keith Hyland Hoa K. Nguyen Robert R. Kane 《Journal of labelled compounds & radiopharmaceuticals》2003,46(5):389-394
Concise methods for the synthesis of 4‐hydroxy‐3‐[2H3]‐methoxyphenylalanine (3‐O‐[2H3]‐methydopa) and 3‐hydroxy‐4‐[2H3]‐methoxyphenylalanine (4‐O‐[2H3]‐methydopa) are described. The 3‐O‐[2H3]‐methydopa is a valuable internal standard for the tandem MS quantification of 3‐O‐methyldopa, a metabolite of value in the diagnosis of aromatic l‐amino acid decarboxylase (AADC) deficiency. Copyright © 2003 John Wiley & Sons, Ltd. 相似文献
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10.
Anh-Hoa Nguyen Pham Kim-Oanh Bui Thi Mai-Huong Nguyen Thi Diem-Ngoc Ngo Nakayuki Naritaka Hiroshi Nittono Hisamitsu Hayashi Trang Thi Dao Kim-Huong Thi Nguyen Hoai-Nghia Nguyen Hoa Giang Hung-Sang Tang Tat-Thanh Nguyen Dinh-Kiet Truong Minh-Dien Tran 《Medicine》2022,101(25)
Rationale:Congenital bile acid synthesis defect (BASD) is a rare disease caused by mutations in the aldo-keto reductase 1D1 gene, which encodes the primary Δ4-3-oxosteroid 5β-reductase enzyme. Early disease diagnosis is critical for early treatment with bile acid replacement therapy, with an excellent chance for recovery. In contrast, protracted diagnosis and treatment may lead to poor outcomes, including decompensated hepatic cirrhosis, liver transplant, and even death.Patient concerns:Three clinical congenital bile acid synthesis defect cases in the Vietnamese population are herein reported. These pediatric patients presented with symptoms of prolonged postpartum jaundice and abnormal loose stool (mucus, lipids, and white). The clinical examinations showed hepatosplenomegaly. Urinalysis showed a very low fraction of primary bile acids and atypical 3-oxo-Δ4- bile acids in all three patients.Diagnoses:The patients were diagnosed with primary Δ4-3-oxosteroid 5β-reductase deficiency. Next-generation gene sequencing revealed two homozygous mutations in the aldo-keto reductase family 1 member D1 gene. The first is a documented variant, c.797G>A (p.Arg266Gln), and the second is a novel mutation at c.155T>C (p.Ile52Thr).Interventions:Immediately after diagnosis, patients were treated with oral chenodeoxycholate 5 mg/kg/d.Outcomes:The patients’ symptoms, signs, and primary bile acids levels improved significantly.Lessons:Clinicians should consider genetic disorders related to cholestasis for effective and life-saving treatment. A prompt genetic analysis by next-generation gene sequencing enables patients to access bile acid replacement therapy earlier, significantly improving short- and long-term outcomes. 相似文献