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

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. The purpose of this investigation was to examine the impact and mechanisms of a...

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Veröffentlicht in:The Science of the total environment 2024-02, Vol.912, p.169613-169613, Article 169613
Hauptverfasser: Peng, Qi, Wu, Yang, Li, Yan, Lu, Chan, Yao, Runming, Hu, Siyuan, Ma, Ning, Chen, Shaohui, Yang, Xu, Ma, Ping
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container_issue
container_start_page 169613
container_title The Science of the total environment
container_volume 912
creator Peng, Qi
Wu, Yang
Li, Yan
Lu, Chan
Yao, Runming
Hu, Siyuan
Ma, Ning
Chen, Shaohui
Yang, Xu
Ma, Ping
description 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. The purpose of this investigation was to examine the impact and mechanisms of allergic asthma exacerbation through the dermal exposure to DINP. 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. 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. 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. [Display omitted] Dermal exposure to DINP aggravates allergic asthma in Balb/c mice.IL-31/TRPV1 pathway is involved in allergic asthma exacerbated by DINP.Dermal exposure to DINP triggers a Th1/Th2 immune imbalance in Balb/c mice.SB-431542 or capsazepine treatment can alleviate allergic asthma exacerbated by DINP.
doi_str_mv 10.1016/j.scitotenv.2023.169613
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However, the current findings do not provide enough evidence to support this claim. The purpose of this investigation was to examine the impact and mechanisms of allergic asthma exacerbation through the dermal exposure to DINP. 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. 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. 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. [Display omitted] Dermal exposure to DINP aggravates allergic asthma in Balb/c mice.IL-31/TRPV1 pathway is involved in allergic asthma exacerbated by DINP.Dermal exposure to DINP triggers a Th1/Th2 immune imbalance in Balb/c mice.SB-431542 or capsazepine treatment can alleviate allergic asthma exacerbated by DINP.</description><identifier>ISSN: 0048-9697</identifier><identifier>EISSN: 1879-1026</identifier><identifier>DOI: 10.1016/j.scitotenv.2023.169613</identifier><identifier>PMID: 38154627</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>adjuvants ; Allergic asthma ; antagonists ; asthma ; biomarkers ; compliance ; Dermal exposure ; Diisononyl phthalate (DINP) ; environment ; histopathology ; immunoglobulins ; inflammation ; interleukin-13 ; Interleukin-31 (IL-31) ; interleukin-4 ; interleukin-5 ; interleukin-6 ; lungs ; phthalates ; Transient receptor potential vanilloid 1 (TRPV1) ; transient receptor potential vanilloid channels</subject><ispartof>The Science of the total environment, 2024-02, Vol.912, p.169613-169613, Article 169613</ispartof><rights>2023</rights><rights>Copyright © 2023. 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[Display omitted] Dermal exposure to DINP aggravates allergic asthma in Balb/c mice.IL-31/TRPV1 pathway is involved in allergic asthma exacerbated by DINP.Dermal exposure to DINP triggers a Th1/Th2 immune imbalance in Balb/c mice.SB-431542 or capsazepine treatment can alleviate allergic asthma exacerbated by DINP.</description><subject>adjuvants</subject><subject>Allergic asthma</subject><subject>antagonists</subject><subject>asthma</subject><subject>biomarkers</subject><subject>compliance</subject><subject>Dermal exposure</subject><subject>Diisononyl phthalate (DINP)</subject><subject>environment</subject><subject>histopathology</subject><subject>immunoglobulins</subject><subject>inflammation</subject><subject>interleukin-13</subject><subject>Interleukin-31 (IL-31)</subject><subject>interleukin-4</subject><subject>interleukin-5</subject><subject>interleukin-6</subject><subject>lungs</subject><subject>phthalates</subject><subject>Transient receptor potential vanilloid 1 (TRPV1)</subject><subject>transient receptor potential vanilloid channels</subject><issn>0048-9697</issn><issn>1879-1026</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqFkUtvEzEQgC0EoqHwF8BHLpt47H3Yx1AoRIpohUKvlteeJY72EWynkP56HKX0Wh_Gh_nmofkI-QBsDgzqxW4erU9TwvF-zhkXc6hVDeIFmYFsVAGM1y_JjLFSFqpWzQV5E-OO5ddIeE0uhISqrHkzI2GzRbpaFwIWmx-3d0D3Jm3_mCMd0HmTMFLT9xh-eUtNTNvBUPxrLIY25xxtj_Tz6vstdRgG0-fUfoqHgNSP9OZuWUQco0_-IZOfTN8uLB28xbfkVWf6iO8e_0vy8_rL5upbsb75urpargtbsjIVMu9dOSmd7VxVCqMaQGdk3cnatMyBVU1TWV6pVlkjZNd1psqRtwoEAybEJfl47rsP0-8DxqQHHy32vRlxOkQtWMlEoxSDZ1GumAQuOK8y2pxRG6YYA3Z6H_xgwlED0yc3eqef3OiTG312kyvfPw45tPm6T3X_ZWRgeQYwX-XeYzg1wtFmEwFt0m7yzw75B2pRo1Q</recordid><startdate>20240220</startdate><enddate>20240220</enddate><creator>Peng, Qi</creator><creator>Wu, Yang</creator><creator>Li, Yan</creator><creator>Lu, Chan</creator><creator>Yao, Runming</creator><creator>Hu, Siyuan</creator><creator>Ma, Ning</creator><creator>Chen, Shaohui</creator><creator>Yang, Xu</creator><creator>Ma, Ping</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20240220</creationdate><title>The IL-31/TRPV1 pathway mediates allergic asthma exacerbated by DINP dermal exposure in OVA-sensitized Balb/c mice</title><author>Peng, Qi ; 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However, the current findings do not provide enough evidence to support this claim. The purpose of this investigation was to examine the impact and mechanisms of allergic asthma exacerbation through the dermal exposure to DINP. 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. 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. 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. [Display omitted] Dermal exposure to DINP aggravates allergic asthma in Balb/c mice.IL-31/TRPV1 pathway is involved in allergic asthma exacerbated by DINP.Dermal exposure to DINP triggers a Th1/Th2 immune imbalance in Balb/c mice.SB-431542 or capsazepine treatment can alleviate allergic asthma exacerbated by DINP.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>38154627</pmid><doi>10.1016/j.scitotenv.2023.169613</doi><tpages>1</tpages></addata></record>
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source Elsevier ScienceDirect Journals
subjects adjuvants
Allergic asthma
antagonists
asthma
biomarkers
compliance
Dermal exposure
Diisononyl phthalate (DINP)
environment
histopathology
immunoglobulins
inflammation
interleukin-13
Interleukin-31 (IL-31)
interleukin-4
interleukin-5
interleukin-6
lungs
phthalates
Transient receptor potential vanilloid 1 (TRPV1)
transient receptor potential vanilloid channels
title The IL-31/TRPV1 pathway mediates allergic asthma exacerbated by DINP dermal exposure in OVA-sensitized Balb/c mice
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