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Research Article
Keiko Kan-o
Department of Endoscopic Diagnostics and Therapeutics, Kyushu University Hospital, Fukuoka, Japan
Corresponding Author
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Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway dysfunction. Using mouse and cell culture models, we evaluated the effects of IS exposure on airway function, such as airway hyperresponsiveness (AHR), expression of multiple epithelial tight junction (TJ)- and adherens junction-associated mRNAs and proteins in the lungs, and the barrier function of bronchial epithelial cells assessed by transepithelial electronic resistance (TEER). Exposure of BALB/c mice to IS increased AHR and inflammatory macrophage recruitment to BALF; reduced claudin-1, -2, -3, -7, -10b, -12, -15, and -18, occludin, zonula occludens-1 [ZO-1], and E-cadherin mRNA expression; and caused discontinuity of claudin-2 and ZO-1 protein immunostaining in lung tissue. IS extract dose-dependently decreased TEER and increased reactive oxygen species production in bronchial epithelial cell cultures. Treatment with N-acetyl-l-cysteine, but not glucocorticosteroids or long-acting β2-agonists, prevented the detrimental effects of IS. IS exposure can be problematic for respiratory health, as evidenced by AHR, increased recruitment of inflammatory macrophages and disruption of TJ proteins in the lung, and damage to epithelial barrier integrity. However, antioxidants may be useful for the treatment of IS-induced airway dysfunction.
Keywords
Incense smoke (IS), transepithelial electronic resistance (TEER), airway hyperresponsiveness (AHR), airway dysfunction
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View the published article at Scientific Reports.
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Posted 04 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 01 Feb, 2021
Reviews received
Received 26 Jan, 2021
Reviewers agreed
On 24 Jan, 2021
Reviewers agreed
On 05 Jan, 2021
Reviewers invited
Invitations sent on 29 Dec, 2020
Editor assigned
On 29 Dec, 2020
Editor invited
On 29 Dec, 2020
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On 28 Dec, 2020
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On 17 Dec, 2020
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Subject Areas
Pulmonology
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A new preprint design is coming!
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See the published version of this preprint at Scientific Reports.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Keiko Kan-o
Department of Endoscopic Diagnostics and Therapeutics, Kyushu University Hospital, Fukuoka, Japan
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Scientific Reports.
Version 1
Posted 04 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 01 Feb, 2021
Reviews received
Received 26 Jan, 2021
Reviewers agreed
On 24 Jan, 2021
Reviewers agreed
On 05 Jan, 2021
Reviewers invited
Invitations sent on 29 Dec, 2020
Editor assigned
On 29 Dec, 2020
Editor invited
On 29 Dec, 2020
Submission checks complete
On 28 Dec, 2020
First submitted
On 17 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Pulmonology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Scientific Reports.
Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway dysfunction. Using mouse and cell culture models, we evaluated the effects of IS exposure on airway function, such as airway hyperresponsiveness (AHR), expression of multiple epithelial tight junction (TJ)- and adherens junction-associated mRNAs and proteins in the lungs, and the barrier function of bronchial epithelial cells assessed by transepithelial electronic resistance (TEER). Exposure of BALB/c mice to IS increased AHR and inflammatory macrophage recruitment to BALF; reduced claudin-1, -2, -3, -7, -10b, -12, -15, and -18, occludin, zonula occludens-1 [ZO-1], and E-cadherin mRNA expression; and caused discontinuity of claudin-2 and ZO-1 protein immunostaining in lung tissue. IS extract dose-dependently decreased TEER and increased reactive oxygen species production in bronchial epithelial cell cultures. Treatment with N-acetyl-l-cysteine, but not glucocorticosteroids or long-acting β2-agonists, prevented the detrimental effects of IS. IS exposure can be problematic for respiratory health, as evidenced by AHR, increased recruitment of inflammatory macrophages and disruption of TJ proteins in the lung, and damage to epithelial barrier integrity. However, antioxidants may be useful for the treatment of IS-induced airway dysfunction.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
This is a list of supplementary files associated with this preprint. Click to download.
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