Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome

BackgroundChildren with Down Syndrome (DS) are at high risk for severe respiratory syncytial virus (RSV) infections. DS is associated with impaired cellular responses to oxidative stress and hypoxia; however, these abnormalities have not been explored in trisomy 21 (TS21) airway epithelial cells (AE...

Full description

Saved in:
Bibliographic Details
Main Authors: Allison Welham, Elizabeth Chorvinsky, Surajit Bhattacharya, Kyle Salka, Betelehem Solomon Bera, Woudasie Admasu, Maria C. Straker, Maria J. Gutierrez, Jyoti K. Jaiswal, Gustavo Nino
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-05-01
Series:Frontiers in Pediatrics
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fped.2025.1553571/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850261488518823936
author Allison Welham
Allison Welham
Allison Welham
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Surajit Bhattacharya
Surajit Bhattacharya
Surajit Bhattacharya
Kyle Salka
Betelehem Solomon Bera
Betelehem Solomon Bera
Betelehem Solomon Bera
Woudasie Admasu
Woudasie Admasu
Woudasie Admasu
Maria C. Straker
Maria C. Straker
Maria C. Straker
Maria J. Gutierrez
Jyoti K. Jaiswal
Jyoti K. Jaiswal
Gustavo Nino
Gustavo Nino
Gustavo Nino
author_facet Allison Welham
Allison Welham
Allison Welham
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Surajit Bhattacharya
Surajit Bhattacharya
Surajit Bhattacharya
Kyle Salka
Betelehem Solomon Bera
Betelehem Solomon Bera
Betelehem Solomon Bera
Woudasie Admasu
Woudasie Admasu
Woudasie Admasu
Maria C. Straker
Maria C. Straker
Maria C. Straker
Maria J. Gutierrez
Jyoti K. Jaiswal
Jyoti K. Jaiswal
Gustavo Nino
Gustavo Nino
Gustavo Nino
author_sort Allison Welham
collection DOAJ
description BackgroundChildren with Down Syndrome (DS) are at high risk for severe respiratory syncytial virus (RSV) infections. DS is associated with impaired cellular responses to oxidative stress and hypoxia; however, these abnormalities have not been explored in trisomy 21 (TS21) airway epithelial cells (AECs) during RSV infection. Understanding these defects is key to identifying factors contributing to severe RSV infections in this high-risk group.MethodsAECs from children with and without DS were analyzed at baseline and after RSV infection to assess NRF2-induced protective genes against oxidative stress and hypoxia, including the enzyme heme oxygenase 1 (HO-1). To investigate DS-specific defects, we focused on miR-155 and BACH1, which regulate NRF2 signaling and HO-1 expression, and are both encoded on chromosome 21. RNA-seq analyses were performed to examine genome-wide hypoxia-related gene responses in control and TS21 AECs at baseline and after RSV infection.ResultsOur findings show that miR-155 inhibits BACH1, leading to increased NRF2-driven HO-1 expression in euploid AECs. In contrast, TS21 AECs from children with DS exhibited impaired HO-1 induction following miR-155 treatment. This was attributed to reduced transcription of the HMOX1 gene, which encodes HO-1, along with global downregulation of hypoxia response genes in DS at baseline and after RSV infection in TS21 AECs.ConclusionsSevere RSV infections in children with DS may be linked to intrinsic defects in AEC responses to hypoxia, including NRF2-driven cytoprotective enzymes like HO-1. These findings offer new mechanistic insights into RSV pathophysiology and potential therapeutic targets in children with DS.
format Article
id doaj-art-acdc62110f564ea9ac4e22d59fdebec8
institution OA Journals
issn 2296-2360
language English
publishDate 2025-05-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Pediatrics
spelling doaj-art-acdc62110f564ea9ac4e22d59fdebec82025-08-20T01:55:22ZengFrontiers Media S.A.Frontiers in Pediatrics2296-23602025-05-011310.3389/fped.2025.15535711553571Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndromeAllison Welham0Allison Welham1Allison Welham2Elizabeth Chorvinsky3Elizabeth Chorvinsky4Elizabeth Chorvinsky5Surajit Bhattacharya6Surajit Bhattacharya7Surajit Bhattacharya8Kyle Salka9Betelehem Solomon Bera10Betelehem Solomon Bera11Betelehem Solomon Bera12Woudasie Admasu13Woudasie Admasu14Woudasie Admasu15Maria C. Straker16Maria C. Straker17Maria C. Straker18Maria J. Gutierrez19Jyoti K. Jaiswal20Jyoti K. Jaiswal21Gustavo Nino22Gustavo Nino23Gustavo Nino24Division of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesJacobs School of Medicine and Biomedical Sciences, University of Buffalo, Buffalo, NY, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Allergy, Immunology and Rheumatology, Johns Hopkins University, Baltimore, MD, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesDivision of Pediatric Pulmonary and Sleep Medicine, Children’s National Hospital, Washington, DC, United StatesCenter for Genetic Medicine Research, Children’s National Research Institute, Washington, DC, United StatesDepartment of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC, United StatesBackgroundChildren with Down Syndrome (DS) are at high risk for severe respiratory syncytial virus (RSV) infections. DS is associated with impaired cellular responses to oxidative stress and hypoxia; however, these abnormalities have not been explored in trisomy 21 (TS21) airway epithelial cells (AECs) during RSV infection. Understanding these defects is key to identifying factors contributing to severe RSV infections in this high-risk group.MethodsAECs from children with and without DS were analyzed at baseline and after RSV infection to assess NRF2-induced protective genes against oxidative stress and hypoxia, including the enzyme heme oxygenase 1 (HO-1). To investigate DS-specific defects, we focused on miR-155 and BACH1, which regulate NRF2 signaling and HO-1 expression, and are both encoded on chromosome 21. RNA-seq analyses were performed to examine genome-wide hypoxia-related gene responses in control and TS21 AECs at baseline and after RSV infection.ResultsOur findings show that miR-155 inhibits BACH1, leading to increased NRF2-driven HO-1 expression in euploid AECs. In contrast, TS21 AECs from children with DS exhibited impaired HO-1 induction following miR-155 treatment. This was attributed to reduced transcription of the HMOX1 gene, which encodes HO-1, along with global downregulation of hypoxia response genes in DS at baseline and after RSV infection in TS21 AECs.ConclusionsSevere RSV infections in children with DS may be linked to intrinsic defects in AEC responses to hypoxia, including NRF2-driven cytoprotective enzymes like HO-1. These findings offer new mechanistic insights into RSV pathophysiology and potential therapeutic targets in children with DS.https://www.frontiersin.org/articles/10.3389/fped.2025.1553571/fulltrisomy 21 (Down syndrome)RSV (respiratory syncytial virus)airway epitheliamiR-155hypoxia
spellingShingle Allison Welham
Allison Welham
Allison Welham
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Elizabeth Chorvinsky
Surajit Bhattacharya
Surajit Bhattacharya
Surajit Bhattacharya
Kyle Salka
Betelehem Solomon Bera
Betelehem Solomon Bera
Betelehem Solomon Bera
Woudasie Admasu
Woudasie Admasu
Woudasie Admasu
Maria C. Straker
Maria C. Straker
Maria C. Straker
Maria J. Gutierrez
Jyoti K. Jaiswal
Jyoti K. Jaiswal
Gustavo Nino
Gustavo Nino
Gustavo Nino
Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
Frontiers in Pediatrics
trisomy 21 (Down syndrome)
RSV (respiratory syncytial virus)
airway epithelia
miR-155
hypoxia
title Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
title_full Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
title_fullStr Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
title_full_unstemmed Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
title_short Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome
title_sort impaired airway epithelial mir 155 bach1 nrf2 axis and hypoxia gene expression during rsv infection in children with down syndrome
topic trisomy 21 (Down syndrome)
RSV (respiratory syncytial virus)
airway epithelia
miR-155
hypoxia
url https://www.frontiersin.org/articles/10.3389/fped.2025.1553571/full
work_keys_str_mv AT allisonwelham impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT allisonwelham impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT allisonwelham impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT elizabethchorvinsky impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT elizabethchorvinsky impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT elizabethchorvinsky impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT surajitbhattacharya impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT surajitbhattacharya impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT surajitbhattacharya impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT kylesalka impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT betelehemsolomonbera impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT betelehemsolomonbera impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT betelehemsolomonbera impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT woudasieadmasu impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT woudasieadmasu impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT woudasieadmasu impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT mariacstraker impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT mariacstraker impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT mariacstraker impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT mariajgutierrez impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT jyotikjaiswal impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT jyotikjaiswal impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT gustavonino impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT gustavonino impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome
AT gustavonino impairedairwayepithelialmir155bach1nrf2axisandhypoxiageneexpressionduringrsvinfectioninchildrenwithdownsyndrome