Bibliographic Details
Title: |
Myeloid-derived suppressor cells exacerbate poly(I:C)-induced lung inflammation in mice with renal injury and older mice |
Authors: |
Zhiqi Xie, Haoyang Zhou, Masanori Obana, Yasushi Fujio, Naoki Okada, Masashi Tachibana |
Source: |
Frontiers in Immunology, Vol 14 (2023) |
Publisher Information: |
Frontiers Media S.A., 2023. |
Publication Year: |
2023 |
Collection: |
LCC:Immunologic diseases. Allergy |
Subject Terms: |
MDSC, poly(I:C), lung inflammation, aging, renal ischemia/reperfusion injury, Immunologic diseases. Allergy, RC581-607 |
More Details: |
Viral pneumonia is a global health burden with a high mortality rate, especially in the elderly and in patients with underlying diseases. Recent studies have found that myeloid-derived suppressor cells (MDSCs) are abundant in these patient groups; however, their roles in the progression of viral pneumonia remain unclear. In this study, we observed a substantial increase in MDSCs in a mouse model of renal ischemia/reperfusion (I/R) injury and in older mice. When intranasal polyinosinic-polycytidylic acid (poly(I:C)) administration was used to mimic viral pneumonia, mice with renal I/R injury exhibited more severe lung inflammation than sham mice challenged with poly(I:C). In addition, MDSC depletion attenuated lung inflammation in mice with I/R injury. Similar results were obtained in older mice compared with those in young mice. Furthermore, adoptive transfer of in vitro-differentiated MDSCs exacerbated poly(I:C)-induced lung inflammation. Taken together, these experimental results suggest that the increased proportion of MDSCs in mice with renal I/R injury and in older mice exacerbates poly(I:C)-induced lung inflammation. These findings have important implications for the treatment and prevention of severe lung inflammation caused by viral pneumonia. |
Document Type: |
article |
File Description: |
electronic resource |
Language: |
English |
ISSN: |
1664-3224 |
Relation: |
https://www.frontiersin.org/articles/10.3389/fimmu.2023.1243851/full; https://doaj.org/toc/1664-3224 |
DOI: |
10.3389/fimmu.2023.1243851 |
Access URL: |
https://doaj.org/article/1150503fdf7748678a7316623385c4d2 |
Accession Number: |
edsdoj.1150503fdf7748678a7316623385c4d2 |
Database: |
Directory of Open Access Journals |