Myeloid-derived suppressor cells exacerbate poly(I:C)-induced lung inflammation in mice with renal injury and older mice

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
More Details
ISSN:16643224
DOI:10.3389/fimmu.2023.1243851
Published in:Frontiers in Immunology
Language:English