• Title/Summary/Keyword: human bronchial epithelial cells

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Differential gene expression by chrysotile in human bronchial epithelial cells

  • Seo, Yoo-Na;Lee, Yong-Jin;Lee, Mi-Young
    • Animal cells and systems
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    • v.16 no.2
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    • pp.95-103
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    • 2012
  • Asbestos exposure has been known to contribute to several lung diseases named asbestosis, malignant mesothelioma and lung cancer, but the disease-related molecular and cellular mechanisms are still largely unknown. To examine the effects of asbestos exposure in human bronchial epithelial cells at gene level, the global gene expression profile was analyzed following chrysotile treatment. The microarray results revealed differential gene expression in response to chrysotile treatment. The genes up- and down-regulated by chrysotile were mainly involved in processes including metabolism, signal transduction, transport, development, transcription, immune response, and other functions. The differential gene expression profiles could provide clues that might be used to understand the pathological mechanisms and therapeutic targets involved in chrysotile-related diseases.

Cytotoxicity of Copper Nanoparticles in Cultured Human Bronchial Epithelial Cells (BEAS-2B) (구리로 만든 나노입자의 기관지상피세포에 미치는 독성)

  • Park Eun-Jung;Park Kwangsik
    • Toxicological Research
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    • v.21 no.4
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    • pp.303-307
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    • 2005
  • Nanomaterials, which ranges in size from 1 to 100 nm, have been used to create uqnique devices at the nanoscale level possessing novel physical and chemical functional properties. However, the toxicities of nanomaterials have not been fully tested and the risk of nanomaterials is emerging issues in these days. In this study, the cytotoxicity of copper nanoparticles was tested in cultured human bronchial epithelial cells. As a results, copper nanoparticles showed cytotoxicity similar with cupric ion and the apoptotic mechanisms of DNA fragmentation and caspase-3 activation were involved. Induction of heme oxygenase-1 and thioredoxin reductase by copper nanoparticles indicated that cytotoxicity of copper nanoparticles is likely to be mediated through oxidative stress.

Effect of Youn-Gyo-Pae-Doc-San on the Release of Thymus and Activation-Regulated Chemokine(TARC) in Human Bronchial Epithelial Cell (連翹敗毒散이 사람 기관지 상피세포의 TARC 분비에 미치는 효과)

  • Lee, Kyung-yeob;Kim, Hee-taek;Kim, E-hwa;Nam, Chang-gyu;Ryu, Ju-hyun
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.16 no.3
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    • pp.82-95
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    • 2003
  • Chemokines are important for the recruitment of leukocytes to sites of infection, which is essential in host defense. The thymus and activation-regulated chemokine (TARC) is a CC chemokine which potentially plays a role via a paracrine mechanism in the development of allergic respiratory diseases. Objectives : The objective of this study is to investigate the effect of Youn-Gyo-Pae-Doc-San on the secretion of TARC of human bronchial epithelial cell Methods : Enzyme-linked immunosorbent assay (ELISA) was performed to detect the secretion of TARC. The cytotoxicity was measured by MTT assay. Results : Youn-Gyo-Pae-Doc-San significantly inhibited the secretion of TARC with a dose -dependant manner. The effective dosage did not have the cytotoxicity on human bronchial epithelial cell. Conclusions : Results of our study show that Youn-Gyo-Pae-Doc-San would play an important role in modulation of TARC in human bronchial epithelial cells.

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Induction of Oxidative Stress by Hexavalent Chromium in Human Bronchial Epithelial Cells (BEAS-2B) (배양 기관지 상피세포(BEAS-2B cells)에서 6가 크롬에 의한 산화적 스트레스)

  • Park, Eun-Jung;Kang, Mi-Sun;Kim, Dae-Seon;Park, Kwang-Sik
    • Environmental Analysis Health and Toxicology
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    • v.21 no.4
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    • pp.357-363
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    • 2006
  • Chromium compounds are widely used in diverse industries including pigment manufacturing, painting, metal plating and leather tanning. With the wide uses of chromium, various adverse effects of the compounds on the environment and human health have been reported. Among them, hexavalent chromium [Cr (VI)], which is a carcinogenic heavy metal, has been widely studies. Epidemiological investigations have shown that respiratory cancers had been found in workers who had been occupationally exposed to Cr (VI). In this study, cell toxicity and induction of reactive oxygen species (ROS) by Cr (VI) (1, 2, 4, $8{\mu}M$) in cultured human bronchial epithelial cells were investigated. Exposure of the cells to Cr (VI) led to cell death, ROS increase, and cytosolic caspase-3 activation. The ROS increase was related with the decreased level of GSH. Chromatin condensation and fragmentation were occurred by Cr (VI) when evaluated by DAPI staining or agarose gel electrophoresis of the extracted DNA. Expression of ROS related genes including glutathione S-transferase, heme oxygenase-1, metallothionein were significantly induced in Cr (VI) treated cells. This result suggests the toxicity in cultured cells by Cr (VI) was expressed through the apoptotic process with ROS induction.

Effect of Ephedrae Herbal Acupuncture Solution(EHS) on the Release of Thymus and Activation-Regulated Chemokine (TARC) in Human Bronchial Epithelial Cell (마황(麻黃) 약침액(藥鍼液)이 사람 기관지 상피세포의 TARC 분비에 미치는 효과)

  • Chou, Yu-Shih;Seo, Jung-Chul;Lim, Seong-chul;Jung, Tae-Young;Han, Sang-Won
    • Korean Journal of Acupuncture
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    • v.22 no.1
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    • pp.23-32
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    • 2005
  • Chemokines are important for the recruitment of leukocytes, which is essential in host defense to the sites of infection. The thymus and activation-regulated chemokine (TARC) is a CC chemokine which potentially plays a role via a paracrine mechanism in the development of allergic respiratory diseases. Objectives : The objective of this study is to investigate the effect of Ephedrae Herba Herbal Acupuncture Solution(EHS) on the secretion of TARC of human bronchial epithelial cell. Methods : Enzyme-linked immunosorbent assay (ELISA) was performed to detect the secretion of TARC. The cytotoxicity was measured by MTT assay. Results : EHS significantly inhibited the secretion of TARC with a dose-dependant manner. The effective dosage did not have the cytotoxicity on human bronchial epithelial cell. Conclusion : Results of our study imply that EHS would play an important role in modulation of TARC in human bronchial epithelial cells by MTT assay.

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Screening of toxic potential of graphene family nanomaterials using in vitro and alternative in vivo toxicity testing systems

  • Chatterjee, Nivedita;Yang, Ji Su;Park, Kwangsik;Oh, Seung Min;Park, Jeonggue;Choi, Jinhee
    • Environmental Analysis Health and Toxicology
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    • v.30
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    • pp.7.1-7.7
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    • 2015
  • Objectives The widely promising applications of graphene nanomaterials raise considerable concerns regarding their environmental and human health risk assessment. The aim of the current study was to evaluate the toxicity profiling of graphene family nanano-materials (GFNs) in alternative in vitro and in vivo toxicity testing models. Methods The GFNs used in this study are graphene nanoplatelets ([GNPs]-pristine, carboxylate [COOH] and amide [$NH_2$]) and graphene oxides (single layer [SLGO] and few layers [FLGO]). The human bronchial epithelial cells (Beas2B cells) as in vitro system and the nematode Caenorhabditis elegans as in vivo system were used to profile the toxicity response of GFNs. Cytotoxicity assays, colony formation assay for cellular toxicity and reproduction potentiality in C. elegans were used as end points to evaluate the GFNs' toxicity. Results In general, GNPs exhibited higher toxicity than GOs in Beas2B cells, and among the GNPs the order of toxicity was pristine > $NH_2$ > COOH. Although the order of toxicity of the GNPs was maintained in C. elegans reproductive toxicity, but GOs were found to be more toxic in the worms than GNPs. In both systems, SLGO exhibited profoundly greater dose dependency than FLGO. The possible reason of their differential toxicity lay in their distinctive physicochemical characteristics and agglomeration behavior in the exposure media. Conclusions The present study revealed that the toxicity of GFNs is dependent on the graphene nanomaterial's physical forms, surface functionalizations, number of layers, dose, time of exposure and obviously, on the alternative model systems used for toxicity assessment.

Proteomic Analysis of Cytokine-Like Proteins Secreted from Human Bronchial Epithelial Cells in Response to Pathogenic Bacterial Infection

  • Park, Mi-Ja;Oh, Mi-Jung;Jo, Dong-Hwan;Chin, Mi-Reyoung;Lee, Ji-Yeon;Park, Ji-Woo;Lee, Na-Gyong;Kim, Dae-Kyong
    • Proceedings of the PSK Conference
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    • pp.111.1-111
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    • 2003
  • Bacterial infection is a very complex process in which both pathogens and host cells play crucial roles, and the host cells undergo drastic changes in their physiology, releasing various proteins in response to the pathogenic infection. Human airway epithelial surface serves as a first line of defense against microorganisms and the external environment. It is well known that bronchial epithelial cells secrete various chemokines and cytokines such as IL-6 and IL-8 to cope with various respiratory pathogens. (omitted)

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Proteomic analysis of proteins Secreted by Human Bronchial Epithelial Cells in Response to Pathogenic Bacterial Infections

  • Oh, Mi-Jung;Park, Mi-Ja;Lee, Ji-Yeon;Park, Ji-Woo;Lee, Na-Gyong;Jung, Sung-Yun;Kim, Dae-Kyong
    • Proceedings of the PSK Conference
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    • pp.220-221
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    • 2003
  • Bacterial infection is a very complex process in which both pathogens and host cells play crucial roles, and the host cells undergo drastic changes in their physiology, releasing various proteins in response to the pathogenic infection. Human airway epithelial surface serves as a first line of defense against microorganisms and the external environment. It is well known that bronchial epithelial cells secrete various chemokines and cytokines such as IL-6 and IL-8 to cope with various respiratory pathogens. (omitted)

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The Role of Interleukin 8 and NF(nuclear factor)-κB in Rhinovirus-Induced Airway Inflammation (Rhinovirus 유발성 기도염증반응에서 Interleukin-8과 전사인자 NF(nuclear factor)-κB의 역할에 대한 연구)

  • Yoon, Ho Joo;Kim, Mi Ok;Sohn, Jang Won;Kim, Jung Mogg;Shin, Dong Ho;Park, Sung Soo
    • Tuberculosis and Respiratory Diseases
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    • v.54 no.1
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    • pp.104-113
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    • 2003
  • Background : Rhinovirus(RV) infections frequently trigger dyspnea and paroxysmal cough in adult patients with asthma and are the most prevalent cause of the common cold. However, the mechanisms of a RV-induced airway inflammation is unclear. Since the RV does not directly destroy the airway epithelium, it is presumed that the immune response to the RV contributes to the pathogenesis of the respiratory symptoms. In order to test this hypothesis, this study characterized the time-sequenced alterations in interleukin(IL)-8 elaboration from the human bronchial epithelial cells and evaluated the role of NF(nuclear factor)-${\kappa}B$ in the RV-induced IL-8 production by pretreating the inhibitors of NF-${\kappa}B$ activation. Methods : The ability of RV-infected human bronchial epithelial cells and BEAS-2B cells to produce the IL-8 was compared with the controls. This study infected BEAS-2B cells with the RV14 obtained from the American Type Culture Collection. The supernatants were harvested from the RV infected BEAS-2B cells and the controls at 2hr, 4hr, 6hr, 12hr, 24hr, 48hr from the inoculation time. This study measured the IL-8 concentration using the ELISA kits. In order to elucidate the role of NF-${\kappa}B$ in the RV-induced IL-8 production, the effect of the NF-${\kappa}B$ inhibitors was evaluated on RV-induced IL-8 production. Results: The BEAS-2B cells produced small amounts of IL-8 that accumulated slowly with time in the culture. The RV was a potent stimulator of the IL-8 proteins production by BEAS-2B human bronchial epithelial cells. Antioxidants, N-acetyl-L-cysteine(NAC),\ and pyrrolidine dithiocarbamate(PDTC), blocked the IL-8 elaboration by the RV-infected BEAS-2B cells, which was dose-dependent, but N-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) did not. Conclusion: Some antioxidants inhibited the RV-induced IL-8 production by blocking the NF-${\kappa}B$, which may have a therapeutic potential in asthma.

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells

  • Lee, Kyoung-Hee;Lee, Chang-Hoon;Woo, Jisu;Jeong, Jiyeong;Jang, An-Hee;Yoo, Chul-Gyu
    • Molecules and Cells
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    • v.41 no.4
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    • pp.282-289
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    • 2018
  • Interleukin-17A (IL-17A) is a pro-inflammatory cytokine mainly derived from T helper 17 cells and is known to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) has been considered as a primary risk factor of COPD. However, the interaction between CS and IL-17A and the underlying molecular mechanisms have not been clarified. In the current study, we investigated the effects of cigarette smoke extract (CSE) on IL-17A-induced IL-8 production in human bronchial epithelial cells, and sought to identify the underlying molecular mechanisms. IL-8 production was significantly enhanced following treatment with both IL-17A and CSE, while treatment with either IL-17A or CSE alone caused only a slight increase in IL-8 production. CSE increased the transcription of IL-17RA/RC and surface membrane expression of IL-17R, which was suppressed by an inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt pathway (LY294002). CSE caused inactivation of glycogen synthase $kinase-3{\beta}$ ($GSK-3{\beta}$) via the PI3K/Akt pathway. Blockade of $GSK-3{\beta}$ inactivation by overexpression of constitutively active $GSK-3{\beta}$ (S9A) completely suppressed the CSE-induced up-regulation of IL-17R expression and the CSE-induced enhancement of IL-8 secretion. In conclusion, inactivation of $GSK-3{\beta}$ via the PI3K/Akt pathway mediates CSE-induced up-regulation of IL-17R, which contributes to the enhancement of IL-17A-induced IL-8 production.