Cargando…

IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization

BACKGROUND: Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results regarding the relationship between IL35 and ALI are inconsistent. Therefore, we aimed to further determine the function of IL35 in ALI in mice and the potential mechanism in th...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Shengsong, Xia, Jingen, Zhang, Yi, Zhan, Qingyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9244303/
https://www.ncbi.nlm.nih.gov/pubmed/35748972
http://dx.doi.org/10.1007/s11033-022-07293-5
_version_ 1784738495124733952
author Chen, Shengsong
Xia, Jingen
Zhang, Yi
Zhan, Qingyuan
author_facet Chen, Shengsong
Xia, Jingen
Zhang, Yi
Zhan, Qingyuan
author_sort Chen, Shengsong
collection PubMed
description BACKGROUND: Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results regarding the relationship between IL35 and ALI are inconsistent. Therefore, we aimed to further determine the function of IL35 in ALI in mice and the potential mechanism in this paper. MATERIALS AND METHODS: Hematoxylin-eosin (HE) staining and Masson staining were used to evaluate lung injury in mice. Immunohistochemical staining was used to evaluate the expression of IL35 p35, TLR4 and MD2 and the Bax/Bcl2 and p-P65/P65 ratios. The expression levels of IL35 EBi3, CD68, CD206 and MPO were assessed by immunofluorescence staining. RT–PCR was used to examine the expression levels of IL1β and IL6. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was performed to detect apoptotic cells. RESULTS: Overexpression of IL35 alleviated LPS-induced ALI in mice. IL35 overexpression decreased the expression of CD68 and increased the expression of CD206 in mice with ALI. Furthermore, upregulation of IL35 expression obviously reduced the expression of MPO, IL1β and IL6 in the lung tissues of mice with ALI. Mechanistically, IL35 suppressed the TLR4/NFκB-P65 pathway, leading to the promotion of the M1 to M2 macrophage transition and alleviation of inflammation in mice with ALI. CONCLUSIONS: IL35 relieved LPS-induced inflammation and ALI in mice by regulating M1/M2 macrophage polarization and inhibiting the activation of the TLR4/NFκB-P65 pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11033-022-07293-5.
format Online
Article
Text
id pubmed-9244303
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Springer Netherlands
record_format MEDLINE/PubMed
spelling pubmed-92443032022-06-30 IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization Chen, Shengsong Xia, Jingen Zhang, Yi Zhan, Qingyuan Mol Biol Rep Original Article BACKGROUND: Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results regarding the relationship between IL35 and ALI are inconsistent. Therefore, we aimed to further determine the function of IL35 in ALI in mice and the potential mechanism in this paper. MATERIALS AND METHODS: Hematoxylin-eosin (HE) staining and Masson staining were used to evaluate lung injury in mice. Immunohistochemical staining was used to evaluate the expression of IL35 p35, TLR4 and MD2 and the Bax/Bcl2 and p-P65/P65 ratios. The expression levels of IL35 EBi3, CD68, CD206 and MPO were assessed by immunofluorescence staining. RT–PCR was used to examine the expression levels of IL1β and IL6. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was performed to detect apoptotic cells. RESULTS: Overexpression of IL35 alleviated LPS-induced ALI in mice. IL35 overexpression decreased the expression of CD68 and increased the expression of CD206 in mice with ALI. Furthermore, upregulation of IL35 expression obviously reduced the expression of MPO, IL1β and IL6 in the lung tissues of mice with ALI. Mechanistically, IL35 suppressed the TLR4/NFκB-P65 pathway, leading to the promotion of the M1 to M2 macrophage transition and alleviation of inflammation in mice with ALI. CONCLUSIONS: IL35 relieved LPS-induced inflammation and ALI in mice by regulating M1/M2 macrophage polarization and inhibiting the activation of the TLR4/NFκB-P65 pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11033-022-07293-5. Springer Netherlands 2022-06-24 2022 /pmc/articles/PMC9244303/ /pubmed/35748972 http://dx.doi.org/10.1007/s11033-022-07293-5 Text en © The Author(s), under exclusive licence to Springer Nature B.V. 2022 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Original Article
Chen, Shengsong
Xia, Jingen
Zhang, Yi
Zhan, Qingyuan
IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title_full IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title_fullStr IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title_full_unstemmed IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title_short IL35 attenuated LPS-induced acute lung injury by regulating macrophage polarization
title_sort il35 attenuated lps-induced acute lung injury by regulating macrophage polarization
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9244303/
https://www.ncbi.nlm.nih.gov/pubmed/35748972
http://dx.doi.org/10.1007/s11033-022-07293-5
work_keys_str_mv AT chenshengsong il35attenuatedlpsinducedacutelunginjurybyregulatingmacrophagepolarization
AT xiajingen il35attenuatedlpsinducedacutelunginjurybyregulatingmacrophagepolarization
AT zhangyi il35attenuatedlpsinducedacutelunginjurybyregulatingmacrophagepolarization
AT zhanqingyuan il35attenuatedlpsinducedacutelunginjurybyregulatingmacrophagepolarization