2. Academic Validation
  3. The IL-31/TRPV1 pathway mediates allergic asthma exacerbated by DINP dermal exposure in OVA-sensitized Balb/c mice

The IL-31/TRPV1 pathway mediates allergic asthma exacerbated by DINP dermal exposure in OVA-sensitized Balb/c mice

  • Sci Total Environ. 2023 Dec 27:912:169613. doi: 10.1016/j.scitotenv.2023.169613.
Qi Peng 1,  Yang Wu 1,  Yan Li 1,  Chan Lu 2,  Runming Yao 3,  Siyuan Hu 1,  Ning Ma 1,  Shaohui Chen 1,  Xu Yang 4,  Ping Ma 5
Affiliations

Affiliations

  • 1 Key Laboratory of Environmental Related Diseases and One Health, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
  • 2 XiangYa School of Public Health, Central South University, Changsha 410078, China.
  • 3 Joint International Research Laboratory of Green Buildings and Built Environments (Ministry of Education), Chongqing University, Chongqing 400045, China.
  • 4 Key Laboratory of Environmental Related Diseases and One Health, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China; Hubei Industrial Technology Research Institute of Intelligent Health, Xianning 437100, China.
  • 5 Key Laboratory of Environmental Related Diseases and One Health, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China. Electronic address: maping@hbstu.edu.cn.
PMID: 38154627 DOI: 10.1016/j.scitotenv.2023.169613
Abstract

Background: The potential role of dermal exposure diisononyl phthalate (DINP) as an Adjuvant in allergic inflammation and asthma has been suggested. However, the current findings do not provide enough evidence to support this claim.

Objectives: The purpose of this investigation was to examine the impact and mechanisms of allergic asthma exacerbation through the dermal exposure to DINP.

Methods: The study was undertaken using OVA-sensitized mice. Lung histopathology and airway hyperreactivity (AHR) were assessed. Expression levels of immunoglobulins (t-IgE, OVA-IgE and OVA-IgG1), cytokines (IL-31, IL-4, IL-5, IL-6, IL-13 and INF-γ), and TRPV1 were measured. To investigate the mechanism by which allergic asthma worsens due to dermal exposure to DINP, the blockade analysis using the IL-31 antagonist SB-431542 and the TRPV1 antagonist capsazepine (CZP) were performed.

Results: The findings of the study revealed that the simultaneous exposure to DINP and OVA resulted in an increase in inspiratory resistance (Ri) and expiratory resistance (Re), a decrease in the minimum value of lung dynamic compliance (Cldyn), and worsened airway remodeling. Additionally, it was found that this exposure led to an increase in the levels of IL-31 and TRPV1, which are biomarkers of Th2 cytokines (IL-4, IL-5, IL-6, and IL-13), as well as immunoglobulins (Total IgE, OVA-lgE, and OVA-IgG1), while decreasing the biomarker of Th1 cytokines (IFN-γ). However, these impairments showed improvement after the administration of SB-431542 or CZP.

Conclusion: The findings of this research indicate that the IL-31/TRPV1 pathway plays a moderating function in OVA-induced allergic asthma worsened by dermal exposure to DINP.

Keywords

Allergic asthma; Dermal exposure; Diisononyl phthalate (DINP); Interleukin-31 (IL-31); Transient receptor potential vanilloid 1 (TRPV1).

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