EpOME Regulates Staphylococcus Aureus-Induced Allergic Airway Inflammation by Targeting the NF-κB and MAPK Signaling Pathways

Research Article | Open Access

Volume 2025 - 3 | Article ID 263 | http://dx.doi.org/10.51521/JJGASTRO-E401

EpOME Regulates Staphylococcus Aureus-Induced Allergic Airway Inflammation by Targeting the NF-κB and MAPK Signaling Pathways

Academic Editor: John Bose

Received 2024-12-20
Revised 2025-01-16
Accepted 2025-01-18
Published 2025-01-22

Xia Chen¹, Qiang Xiao¹*

¹Department of Pediatrics, Affiliated Hospital of Chengdu University, Chengdu University, Chengdu, Sichuan 610081, China.

*Correspondence: Qiang Xiao, Department of Pediatrics, Affiliated Hospital of Chengdu University, Chengdu University, No.82, North 2 Section, Erhuan Road, Chengdu City, Sichuan 610081, China

Citation: Xia Chen, Qiang Xiao* (2025) EpOME Regulates Staphylococcus Aureus-Induced Allergic Airway Inflammation by Targeting the NF-κB and MAPK Signaling Pathways. IntJ Gastroenterol Hepatol Endosc. 2025 January;1-5.

Copyrights © 2025, Xia Chen, Qiang Xiao. This article is licensed under the Creative Commons Attribution-Non Commercial-4.0-International-License-(CCBY-NC) (bostonsciencepublishing.us). Usage and distribution for commercial purposes require written permission.

Abstract

Allergic airway inflammation (AAI) is a chronic disease caused by immune system dysfunction, leading to serious quality of life impairments such as allergic rhinitis and asthma, especially in children and newborns. Staphylococcus aureus is a common pathogen that plays a crucial role in exacerbating these inflammatory conditions by activating key immune pathways, including NF - κ B and MAPK. This study investigated the potential therapeutic effect of linoleic acid metabolite 9,10-epoxyoctadecenoic acid (EpoME) in regulating allergic airway inflammation induced by Staphylococcus aureus. There are studies suggesting that EpoME may regulate these inflammatory pathways to reduce inflammation, improve airway hyperresponsiveness, and repair epithelial cell damage. In in vivo experiments, we observed that EpoME treatment significantly reduced airway resistance and improved lung compliance in a mouse model, indicating an improvement in airway hyperresponsiveness. In addition, EpoME treatment reduced the levels of pro-inflammatory cytokines such as IL-6, TNF - α, and IL-1 β in serum, highlighting its role in reducing systemic and local inflammation. Western blot analysis confirmed that EpoME inhibits the activation of NF - κ B and MAPK signaling pathways, further supporting its anti-inflammatory effects. These results suggest that EpoME may become a potential therapeutic agent for treating allergic airway inflammation induced by Staphylococcus aureus by targeting these key inflammatory pathways. This study emphasizes the therapeutic potential of EpoME as an anti-inflammatory agent, particularly in cases involving Staphylococcus aureus induced airway inflammation. EpoME may provide a new approach for managing allergic airway diseases, which has great significance for newborns and other susceptible populations.

Keywords

Allergic Airway Inflammation (AAI), 9,10-Epoxyoctadecenoic acid (EpOME), Staphylococcus aureus, NF-κB signaling, MAPK signaling