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Cigarette smoke particles-induced airway hyperreactivity in vivo and in vitro

Zhang, Yaping LU ; Zhang, Han ; Qin, Qiaohong ; Jia, Min and Xu, Cang Bao LU (2019) In Biological and Pharmaceutical Bulletin 42(5). p.703-711
Abstract

Cigarette smoke is a well-known strong risk factor for inducing airway hyperreactivity (AHR), but the underlying molecular mechanisms are not fully understood. In the present study, mouse in-vivo and in-vitro models were used to study effects of dimethyl sulfoxide (DMSO)-extracted cigarette smoke particles (DSP) on the airway, and to explore the underlying molecular mechanisms that are involved in DSP-induced AHR. In mouse in-vivo model, DSP (0.75, 1.5 or 3 μL/mL) was administered intranasally daily for 7 d. At the end of this period, lung functions were measured with flexiVent". The results showed that the mice exhibited AHR in a dose-dependent manner following methacholine inhalation in vivo. In mouse in-vitro organ culture model,... (More)

Cigarette smoke is a well-known strong risk factor for inducing airway hyperreactivity (AHR), but the underlying molecular mechanisms are not fully understood. In the present study, mouse in-vivo and in-vitro models were used to study effects of dimethyl sulfoxide (DMSO)-extracted cigarette smoke particles (DSP) on the airway, and to explore the underlying molecular mechanisms that are involved in DSP-induced AHR. In mouse in-vivo model, DSP (0.75, 1.5 or 3 μL/mL) was administered intranasally daily for 7 d. At the end of this period, lung functions were measured with flexiVent". The results showed that the mice exhibited AHR in a dose-dependent manner following methacholine inhalation in vivo. In mouse in-vitro organ culture model, exposure of mouse tracheal segments to DSP (0.1 μL/mL) with or without the following pharmacological inhibitors: specific c-Jun-N-terminal kinase (JNK) inhibitor SP600125 (10 μM) or the anti-inflammatory drug dexamethasone (1 μM). DSP-induced bradykinin receptor-mediated airway contraction with increased mRNA and protein expressions for bradykinin B1 and B2 receptors could be significantly reduced by SP600125 or dexamethasone. In conclusion, the present study demonstrates that DSP could induce AHR in vivo and in vitro. In addition to this, the upregulation of bradykinin receptors in airway is most likely one of the underlying molecular mechanisms involved.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Airway hyperreactivity, Bradykinin receptor, C-Jun-N-terminal kinase, Cigarette smoke particle, Lung mechanics
in
Biological and Pharmaceutical Bulletin
volume
42
issue
5
pages
9 pages
publisher
The Pharmaceutical Society of Japan
external identifiers
  • scopus:85065654902
  • pmid:31061312
ISSN
0918-6158
DOI
10.1248/bpb.b18-00736
language
English
LU publication?
yes
id
f52a46d6-6f2f-4549-9267-a4a1c4e2aa67
date added to LUP
2019-06-17 14:02:28
date last changed
2024-06-25 18:57:46
@article{f52a46d6-6f2f-4549-9267-a4a1c4e2aa67,
  abstract     = {{<p>Cigarette smoke is a well-known strong risk factor for inducing airway hyperreactivity (AHR), but the underlying molecular mechanisms are not fully understood. In the present study, mouse in-vivo and in-vitro models were used to study effects of dimethyl sulfoxide (DMSO)-extracted cigarette smoke particles (DSP) on the airway, and to explore the underlying molecular mechanisms that are involved in DSP-induced AHR. In mouse in-vivo model, DSP (0.75, 1.5 or 3 μL/mL) was administered intranasally daily for 7 d. At the end of this period, lung functions were measured with flexiVent". The results showed that the mice exhibited AHR in a dose-dependent manner following methacholine inhalation in vivo. In mouse in-vitro organ culture model, exposure of mouse tracheal segments to DSP (0.1 μL/mL) with or without the following pharmacological inhibitors: specific c-Jun-N-terminal kinase (JNK) inhibitor SP600125 (10 μM) or the anti-inflammatory drug dexamethasone (1 μM). DSP-induced bradykinin receptor-mediated airway contraction with increased mRNA and protein expressions for bradykinin B1 and B<sub>2</sub> receptors could be significantly reduced by SP600125 or dexamethasone. In conclusion, the present study demonstrates that DSP could induce AHR in vivo and in vitro. In addition to this, the upregulation of bradykinin receptors in airway is most likely one of the underlying molecular mechanisms involved.</p>}},
  author       = {{Zhang, Yaping and Zhang, Han and Qin, Qiaohong and Jia, Min and Xu, Cang Bao}},
  issn         = {{0918-6158}},
  keywords     = {{Airway hyperreactivity; Bradykinin receptor; C-Jun-N-terminal kinase; Cigarette smoke particle; Lung mechanics}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{703--711}},
  publisher    = {{The Pharmaceutical Society of Japan}},
  series       = {{Biological and Pharmaceutical Bulletin}},
  title        = {{Cigarette smoke particles-induced airway hyperreactivity in vivo and in vitro}},
  url          = {{http://dx.doi.org/10.1248/bpb.b18-00736}},
  doi          = {{10.1248/bpb.b18-00736}},
  volume       = {{42}},
  year         = {{2019}},
}