Effects of nanoparticles on neuroinflammation in a mouse model of asthma

Byeong Gon Kim, Moo Kyun Park, Pureun Haneul Lee, Sun Hye Lee, Jisu Hong, Moh Moh Myint Aung, Khine Thandar Moe, Nyein Yu Han, An Soo Jang

Research output: Contribution to journalArticle

Abstract

The interaction between chronic inflammation and neural dysfunction points to a link between the nervous and immune systems in the airways. In particular, environmental exposure to nanoparticles (NPs), defined as particulate matter having one dimension <100 nm, is associated with an enhanced risk of childhood and adult asthma. However, the impact of NPs on the neural response in asthma remains to be determined. This study determined the impact of NPs on neuroinflammation in a mouse model of allergic asthma. Ovalbumin (OVA) sensitized mice were treated with saline (Sham), OVA challenged and exposed to 200 μg/m3 NPs 1 h a day for 3 days on days 21–23 in a closed-system chamber attached to a ultrasonic nebulizer. The effect of NPs on the levels of neuropeptides, transient receptor potential vanilloid 1 (TRPV1), TRPV4, P2 × 4, and P2 × 7 was assessed by enzyme-linked immunosorbent assays, immunoblotting, and immunohistochemistry. NP exposure increased airway inflammation and responsiveness in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. The lung tissue levels of TRPV1, TRPV4, P2 × 4, and P2 × 7 were increased in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. The substance P, adenosine triphosphate (ATP), and calcitonin gene-related peptide (CGRP) levels in bronchoalveolar lavage fluid were increased in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. Bradykinin, ATP, and CGRP were dose dependently increased in NP-exposed normal human bronchial epithelial (NHBE) cells. The calcium concentration was increased in NHBE cells exposed to NPs for 8 h. These results indicate that neuroinflammation can be involved in the pathogenesis of bronchial asthma and that NPs can exacerbate asthma via neuromediator release.

Original languageEnglish
Article number103292
JournalRespiratory Physiology and Neurobiology
Volume271
DOIs
StatePublished - Jan 2020

Fingerprint

Nanoparticles
Asthma
Ovalbumin
Calcitonin Gene-Related Peptide
Adenosine Triphosphate
Epithelial Cells
Neuropeptide Receptors
Inflammation
Particulate Matter
Nebulizers and Vaporizers
Environmental Exposure
Bronchoalveolar Lavage Fluid
Bradykinin
Substance P
Immunoblotting
Ultrasonics
Nervous System
Immune System
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry

Keywords

  • Air pollution
  • Bronchial asthma
  • Nanoparticles
  • Neuroinflammation
  • Titanium dioxide

Cite this

Kim, Byeong Gon ; Park, Moo Kyun ; Lee, Pureun Haneul ; Lee, Sun Hye ; Hong, Jisu ; Aung, Moh Moh Myint ; Moe, Khine Thandar ; Han, Nyein Yu ; Jang, An Soo. / Effects of nanoparticles on neuroinflammation in a mouse model of asthma. In: Respiratory Physiology and Neurobiology. 2020 ; Vol. 271.
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Effects of nanoparticles on neuroinflammation in a mouse model of asthma. / Kim, Byeong Gon; Park, Moo Kyun; Lee, Pureun Haneul; Lee, Sun Hye; Hong, Jisu; Aung, Moh Moh Myint; Moe, Khine Thandar; Han, Nyein Yu; Jang, An Soo.

In: Respiratory Physiology and Neurobiology, Vol. 271, 103292, 01.2020.

Research output: Contribution to journalArticle

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T1 - Effects of nanoparticles on neuroinflammation in a mouse model of asthma

AU - Kim, Byeong Gon

AU - Park, Moo Kyun

AU - Lee, Pureun Haneul

AU - Lee, Sun Hye

AU - Hong, Jisu

AU - Aung, Moh Moh Myint

AU - Moe, Khine Thandar

AU - Han, Nyein Yu

AU - Jang, An Soo

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AB - The interaction between chronic inflammation and neural dysfunction points to a link between the nervous and immune systems in the airways. In particular, environmental exposure to nanoparticles (NPs), defined as particulate matter having one dimension <100 nm, is associated with an enhanced risk of childhood and adult asthma. However, the impact of NPs on the neural response in asthma remains to be determined. This study determined the impact of NPs on neuroinflammation in a mouse model of allergic asthma. Ovalbumin (OVA) sensitized mice were treated with saline (Sham), OVA challenged and exposed to 200 μg/m3 NPs 1 h a day for 3 days on days 21–23 in a closed-system chamber attached to a ultrasonic nebulizer. The effect of NPs on the levels of neuropeptides, transient receptor potential vanilloid 1 (TRPV1), TRPV4, P2 × 4, and P2 × 7 was assessed by enzyme-linked immunosorbent assays, immunoblotting, and immunohistochemistry. NP exposure increased airway inflammation and responsiveness in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. The lung tissue levels of TRPV1, TRPV4, P2 × 4, and P2 × 7 were increased in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. The substance P, adenosine triphosphate (ATP), and calcitonin gene-related peptide (CGRP) levels in bronchoalveolar lavage fluid were increased in OVA mice, and these increases were augmented in OVA plus NP-exposed mice. Bradykinin, ATP, and CGRP were dose dependently increased in NP-exposed normal human bronchial epithelial (NHBE) cells. The calcium concentration was increased in NHBE cells exposed to NPs for 8 h. These results indicate that neuroinflammation can be involved in the pathogenesis of bronchial asthma and that NPs can exacerbate asthma via neuromediator release.

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