BibTex format
@article{Scott:2025:10.1016/j.mucimm.2024.12.001,
author = {Scott, IC and Zuydam, NV and Cann, JA and Negri, VA and Tsafou, K and Killick, H and Liu, Z and McCrae, C and Rees, DG and England, E and Guscott, MA and Houslay, K and McCormick, D and Freeman, A and Schofield, D and Freeman, A and Cohen, ES and Thwaites, R and Brohawn, Z and Platt, A and Openshaw, PJM and Semple, MG and Baillie, JK and Wilkinson, T},
doi = {10.1016/j.mucimm.2024.12.001},
journal = {Mucosal Immunology},
pages = {312--325},
title = {IL-33 is associated with alveolar dysfunction in patients with viral lower respiratory tract disease},
url = {http://dx.doi.org/10.1016/j.mucimm.2024.12.001},
volume = {18},
year = {2025}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Interleukin (IL)-33 is released following tissue damage, causing airway inflammation and remodelling via reduced IL-33 (IL-33red)/serum stimulation-2 (ST2) and oxidised IL-33 (IL-33ox)/receptor for advanced glycation end products (RAGE)/epidermal growth factor receptor (EGFR) pathways. This study aimed to identify associations of IL-33 with clinical outcomes and pathological mechanisms during viral lower respiratory tract disease (LRTD). Ultra-sensitive immunoassays were developed to measure IL-33red, IL-33ox and IL-33/sST2 complexes in samples from patients hospitalised with COVID-19. Immunohistochemistry and multiomics were used to characterise lung samples. Elevated IL-33 in the airway and IL-33/sST2 complex in the circulation correlated with poor clinical outcomes (death, need for intensive care or mechanical ventilation). IL-33 was localised to airway epithelial and endothelial barriers, whereas IL1RL1 was expressed on aerocytes, alveolar endothelial cells specialised for gaseous exchange. IL-33 increased expression of mediators of neutrophilic inflammation, immune cell infiltration, interferon signalling and coagulation in endothelial cell cultures. Endothelial IL-33 signatures were strongly related with signatures associated with viral LRTD. Increased IL-33 release following respiratory viral infections is associated with poor clinical outcomes and might contribute to alveolar dysfunction. Although this does not show a causal relationship with disease, these results provide a rationale to evaluate pathological roles for IL-33 in viral LRTD.
AU - Scott,IC
AU - Zuydam,NV
AU - Cann,JA
AU - Negri,VA
AU - Tsafou,K
AU - Killick,H
AU - Liu,Z
AU - McCrae,C
AU - Rees,DG
AU - England,E
AU - Guscott,MA
AU - Houslay,K
AU - McCormick,D
AU - Freeman,A
AU - Schofield,D
AU - Freeman,A
AU - Cohen,ES
AU - Thwaites,R
AU - Brohawn,Z
AU - Platt,A
AU - Openshaw,PJM
AU - Semple,MG
AU - Baillie,JK
AU - Wilkinson,T
DO - 10.1016/j.mucimm.2024.12.001
EP - 325
PY - 2025///
SN - 1933-0219
SP - 312
TI - IL-33 is associated with alveolar dysfunction in patients with viral lower respiratory tract disease
T2 - Mucosal Immunology
UR - http://dx.doi.org/10.1016/j.mucimm.2024.12.001
UR - https://doi.org/10.1016/j.mucimm.2024.12.001
VL - 18
ER -
