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IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection.

Authors :
Portugal CAA
de Araújo Castro Í
Prates MCM
Gagliardi TB
Martins RB
de Jesus BLS
de Souza Cardoso R
da Silva MVG
Aragon DC
Arruda Neto E
Alves Filho JCF
Cunha FQ
Carlotti APCP
Source :
Cytokine [Cytokine] 2020 Mar; Vol. 127, pp. 154965. Date of Electronic Publication: 2020 Jan 03.
Publication Year :
2020

Abstract

Background: Mechanisms influencing severity of acute lower respiratory infection (ALRI) in children are not established. We aimed to assess the role of inflammatory markers and respiratory viruses in ALRI severity.<br />Methods: Concentrations of interleukin(IL)-33, soluble suppression of tumorigenicity (sST)2, IL-1ß, tumor necrosis factor α, IL-4, IL-6 and IL- 8 and types of respiratory viruses were evaluated in children at the first and fifth days after hospital admission. Disease severity was defined as need for mechanical ventilation.<br />Results: Seventy-nine children <5 years-old were included; 33(41.8%) received mechanical ventilation. No associations between virus type, viral load or co-detections and severity of disease were observed. Detection of IL-33 and sST2 in nasopharyngeal aspirates (NPA) on admission were associated with higher risk for mechanical ventilation (RR = 2.89 and RR = 4.57, respectively). IL-6 and IL-8 concentrations were higher on Day 5 in mechanically ventilated children. IL-6 NPA concentrations decreased from Day 1 to Day 5 in children who did not receive mechanical ventilation. Increase in sST2 NPA concentrations from Day 1 to Day 5 was associated with longer hospital length of stay (p < 0.01).<br />Conclusions: An exacerbated local activation of the IL-33/ST2 axis and persistently high sST2 concentrations over time were associated with severity of viral ALRI in children.<br />Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Details

Language :
English
ISSN :
1096-0023
Volume :
127
Database :
MEDLINE
Journal :
Cytokine
Publication Type :
Academic Journal
Accession number :
31901762
Full Text :
https://doi.org/10.1016/j.cyto.2019.154965