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RISS 인기검색어
- 검색키워드
- 저자 : Mutsuo Yamaya (검색결과 3 건)
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Ambroxol inhibits rhinovirus infection in primary cultures of human tracheal epithelial cells
Yamaya, Mutsuo,Nishimura, Hidekazu,Nadine, Lusamba Kalonji,Ota, Chiharu,Kubo, Hiroshi,Nagatomi, Ryoichi 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.4
The mucolytic drug ambroxol hydrochloride reduces the production of pro-inflammatory cytokines and the frequency of exacerbation in patients with chronic obstructive pulmonary disease (COPD). However, the inhibitory effects of ambroxol on rhinovirus infection, the major cause of COPD exacerbations, have not been studied. We examined the effects of ambroxol on type 14 rhinovirus (RV14) infection, a major RV group, in primary cultures of human tracheal epithelial cells. RV14 infection increased virus titers and cytokine content in the supernatants and RV14 RNA in the cells. Ambroxol (100 nM) reduced RV14 titers and cytokine concentrations of interleukin (IL)-$1{\beta}$, IL-6 and IL-8 in the supernatants and RV14 RNA in the cells after RV14 infection, in addition to reducing susceptibility to RV14 infection. Ambroxol also reduced the expression of intercellular adhesion molecule-1 (ICAM-1), the receptor for RV14, and the number of acidic endosomes from which RV14 RNA enters the cytoplasm. In addition, ambroxol reduced the activation of the transcription factor nuclear factor kappa B (NF-${\kappa}B$) in the nucleus. These results suggest that ambroxol inhibits RV14 infection partly by reducing ICAM-1 and acidic endosomes via the inhibition of NF-${\kappa}B$ activation. Ambroxol may modulate airway inflammation by reducing the production of cytokines in rhinovirus infection.
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Ambroxol inhibits rhinovirus infection in primary cultures of human tracheal epithelial cells
Mutsuo Yamaya,Hidekazu Nishimura,Lusamba Kalonji Nadine,Chiharu Ota,Hiroshi Kubo,Ryoichi Nagatomi 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.4
The mucolytic drug ambroxol hydrochloridereduces the production of pro-inflammatory cytokines andthe frequency of exacerbation in patients with chronicobstructive pulmonary disease (COPD). However, theinhibitory effects of ambroxol on rhinovirus infection, themajor cause of COPD exacerbations, have not been studied. We examined the effects of ambroxol on type 14rhinovirus (RV14) infection, a major RV group, in primarycultures of human tracheal epithelial cells. RV14 infectionincreased virus titers and cytokine content in the supernatantsand RV14 RNA in the cells. Ambroxol (100 nM)reduced RV14 titers and cytokine concentrations of interleukin(IL)-1b, IL-6 and IL-8 in the supernatants and RV14RNA in the cells after RV14 infection, in addition toreducing susceptibility to RV14 infection. Ambroxol alsoreduced the expression of intercellular adhesion molecule-1 (ICAM-1), the receptor for RV14, and the number ofacidic endosomes from which RV14 RNA enters thecytoplasm. In addition, ambroxol reduced the activation ofthe transcription factor nuclear factor kappa B (NF-jB) inthe nucleus. These results suggest that ambroxol inhibitsRV14 infection partly by reducing ICAM-1 and acidicendosomes via the inhibition of NF-jB activation. Ambroxol may modulate airway inflammation by reducingthe production of cytokines in rhinovirus infection.
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Mutsuo Yamaya,Kazuhiro Nomura,Kazuya Arakawa,Mitsuru Sugawara,Xue Deng,Nadine Lusamba Kalonji,Hidekazu Nishimura,Mitsuhiro Yamada,Ryoichi Nagatomi,Tetsuaki Kawase 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.5
Rhinoviral infection is associated with anincreased risk of asthma attacks. The macrolide clarithromycindecreases cytokine production in nasopharyngealaspirates from patients with wheezing, but the effectsof macrolides on cytokine production in nasal epithelialcells obtained from asthmatic subjects remain unclear. Here, human nasal epithelial cells were infected with type-14 rhinovirus (RV14), a major RV group. Titers and RNAof RV14 and cytokine concentrations, including IL-1b andIL-6, were higher in the supernatants of the cells obtainedfrom subjects with bronchial asthma (asthmatic group) thanin those from the non-asthmatic group. Pretreatment withclarithromycin decreased RV14 titers, viral RNA andcytokine concentrations, and susceptibility to RV14infection. Pretreatment with clarithromycin also decreasedIL-33 production, which was detected after infection. Pretreatment with clarithromycin decreased the expressionof intercellular adhesion molecule-1, the receptor forRV14, after infection, the number and fluorescence intensityof the acidic endosomes through which RV RNAenters the cytoplasm, and the activation of nuclear factorkappa-B proteins in nuclear extracts. These findings suggestedthat RV replication and cytokine production may beenhanced in nasal epithelial cells obtained from subjectswith bronchial asthma and may be modulated byclarithromycin.
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