Journal article
Recruitment and training of alveolar macrophages after pneumococcal pneumonia
JCI insight, Vol.7(5), 150239
03/08/2022
DOI: 10.1172/jci.insight.150239
PMCID: PMC8983128
PMID: 35133985
Abstract
Recovery from pneumococcal pneumonia remodels the pool of alveolar macrophages so that they exhibit new surface marker profiles, transcriptomes, metabolomes, and responses to infection. Mechanisms mediating alveolar macrophage phenotypes after pneumococcal pneumonia have not been delineated. IFN-gamma and its receptor on alveolar macrophages were essential for certain, but not all, aspects of the remodeled alveolar macrophage phenotype. IFN-gamma was produced by CD4(+) T cells plus other cells, and CD4(+) cell depletion did not prevent alveolar macrophage remodeling. In mice infected or recovering from pneumococcus, monocytes were recruited to the lungs, and the monocyte-derived macrophages developed characteristics of alveolar macrophages. CCR2 mediated the early monocyte recruitment but was not essential to the development of the remodeled alveolar macrophage phenotype. Lineage tracing demonstrated that recovery from pneumococcal pneumonias converted the pool of alveolar macrophages from being primarily of embryonic origin to being primarily of adult hematopoietic stem cell origin. Alveolar macrophages of either origin demonstrated similar remodeled phenotypes, suggesting that ontogeny did not dictate phenotype. Our data reveal that the remodeled alveolar macrophage phenotype in lungs recovered from pneumococcal pneumonia results from a combination of new recruitment plus training of both the original cells and the new recruits.
Details
- Title: Subtitle
- Recruitment and training of alveolar macrophages after pneumococcal pneumonia
- Creators
- Emad Arafa - Boston UniversityAnukul T. Shenoy - Boston UniversityKimberly A. Barker - Boston UniversityNeelou S. Etesami - Boston UniversityIan M. C. Martin - Boston UniversityCarolina Lyon De Ana - Boston UniversityElim Na - Boston UniversityChristine Odom - Boston UniversityWesley N. Goltry - Boston UniversityFiliz T. Korkmaz - University of Massachusetts Chan Medical SchoolAlicia K. Wooten - Boston UniversityAnna C. Belkina - Boston UniversityAntoine Guillon - InsermE. Camilla Forsberg - University of California, Santa CruzMatthew R. Jones - Boston UniversityLee J. Quinton - Boston UniversityJoseph P. Mizgerd - Boston University
- Resource Type
- Journal article
- Publication Details
- JCI insight, Vol.7(5), 150239
- Publisher
- Amer Soc Clinical Investigation Inc
- DOI
- 10.1172/jci.insight.150239
- PMID
- 35133985
- PMCID
- PMC8983128
- ISSN
- 2379-3708
- eISSN
- 2379-3708
- Number of pages
- 19
- Grant note
- R35 HL135756; R01 AI115053; UL1 TR001430; T32 HL007035; F31 HL-147397 / US NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
- Language
- English
- Date published
- 03/08/2022
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984696756502771
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