Recruitment and training of alveolar macrophages after pneumococcal pneumonia.
Recruitment and training of alveolar macrophages after pneumococcal pneumonia.
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DOI:
10.1172/jci.insight.150239
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发表时间:
2022-03-08
期刊:
影响因子:
8
通讯作者:
Mizgerd JP
中科院分区:
文献类型:
--
作者:
Arafa EI;Shenoy AT;Barker KA;Etesami NS;Martin IM;Lyon De Ana C;Na E;Odom CV;Goltry WN;Korkmaz FT;Wooten AK;Belkina AC;Guillon A;Forsberg EC;Jones MR;Quinton LJ;Mizgerd JP
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-γ and its receptor on alveolar macrophages were essential for certain, but not all, aspects of the remodeled alveolar macrophage phenotype. IFN-γ 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.
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影响因子:
23.9
作者:
Lechner AJ;Driver IH;Lee J;Conroy CM;Nagle A;Locksley RM;Rock JR
通讯作者:
Rock JR
DOI:
10.1084/jem.20162152
发表时间:
2017-08-07
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Misharin AV;Morales-Nebreda L;Reyfman PA;Cuda CM;Walter JM;McQuattie-Pimentel AC;Chen CI;Anekalla KR;Joshi N;Williams KJN;Abdala-Valencia H;Yacoub TJ;Chi M;Chiu S;Gonzalez-Gonzalez FJ;Gates K;Lam AP;Nicholson TT;Homan PJ;Soberanes S;Dominguez S;Morgan VK;Saber R;Shaffer A;Hinchcliff M;Marshall SA;Bharat A;Berdnikovs S;Bhorade SM;Bartom ET;Morimoto RI;Balch WE;Sznajder JI;Chandel NS;Mutlu GM;Jain M;Gottardi CJ;Singer BD;Ridge KM;Bagheri N;Shilatifard A;Budinger GRS;Perlman H
通讯作者:
Perlman H
DOI:
10.1164/rccm.2112012
发表时间:
2002-08-01
影响因子:
24.7
作者:
Maus, U;von Grote, K;Lohmeyer, J
通讯作者:
Lohmeyer, J
影响因子:
8.8
作者:
Leach SM;Gibbings SL;Tewari AD;Atif SM;Vestal B;Danhorn T;Janssen WJ;Wager TD;Jakubzick CV
通讯作者:
Jakubzick CV
DOI:
10.1084/jem.20062648
发表时间:
2007-07-09
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Caton ML;Smith-Raska MR;Reizis B
通讯作者:
Reizis B