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Macrophage Depletion in CCR2(-/-) Mice Delays Bacterial Clearance and Enhances Neutrophil Infiltration in an Acute Otitis Media Modelopen access

Authors
Hur, Dong GuKurabi, ArwaLim, Hyun WooSpriggs, MeghanPak, KwangRyan, Allen F.
Issue Date
15-Jan-2021
Publisher
OXFORD UNIV PRESS INC
Keywords
CCR2; chlodronate liposome; macrophages; otitis media
Citation
JOURNAL OF INFECTIOUS DISEASES, v.223, no.2, pp.333 - 341
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF INFECTIOUS DISEASES
Volume
223
Number
2
Start Page
333
End Page
341
URI
https://scholarworks.bwise.kr/gnu/handle/sw.gnu/4229
DOI
10.1093/infdis/jiaa353
ISSN
0022-1899
Abstract
Background. Otitis media (OM) is a common and potentially serious disease of childhood. Although OM is multifactorial on origin, bacterial infection is a unifying component. Many studies have established a critical role for innate immunity in bacterial clearance and OM resolution. A key component of innate immunity is the recruitment of immune and inflammatory cells, including macrophages. Methods. To explore the role of macrophages in OM, we evaluated the expression of genes related to macrophage function during a complete episode of acute OM in the mouse caused by middle ear (ME) inoculation with Haernophilus influenzae. We also combined CCR2 deficiency with chlodronate liposome toxicity to deplete macrophages during OM. Results. Macrophage genes were robustly regulated during OM. Moreover, macrophage depletion enhanced and prolonged the infiltration of neutrophils into the infected ME and increased the persistence of bacterial infection. Conclusions. The results illustrate the critical role played by macrophages in OM resolution.
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