Literature DB >> 27660037

Immature monocytes contribute to cardiopulmonary bypass-induced acute lung injury by generating inflammatory descendants.

Zhichen Xing1,2, Junyan Han3,4, Xing Hao1,2, Jinhong Wang1,2, Chunjing Jiang1,2, Yu Hao3,4, Hong Wang1,2, Xueying Wu3,4, Liwei Shen5,6, Xiaojun Dong5,6, Tong Li3,4, Guoli Li3,4, Jianping Zhang3,4, Xiaotong Hou1,2, Hui Zeng3,4.   

Abstract

BACKGROUND: As immune regulatory and effector cells, monocytes play an important role in the blood-extracorporeal circuit contact-related acute lung injury in patients undergoing cardiopulmonary bypass (CPB). However, circulating monocytes are phenotypically and functionally heterogeneous, so we characterised how immature monocytes affect acute lung injury induced by CPB.
METHODS: The identification and dynamic changes in monocyte subsets were monitored by flow cytometry in patients undergoing CPB and in a rat model of CPB. The differentiation and migration of monocyte subsets were explored by in vitro cultures and adoptive transfer in the CPB rat model.
RESULTS: We observed a dramatic increase of two monocyte subsets in the peripheral blood of patients undergoing CPB, involving tumour necrosis factor (TNF)-α-producing, mature intermediate CD14highCD16+ monocytes and a novel immature CD14lowCD16- subset. The immature CD14lowCD16- monocytes possessed limited ability for TNF-α production, and failed to suppress T-cell proliferation mediated by T-cell receptor signalling. However, these immature cells were highly proliferative and could differentiate into TNF-α producing, mature CD14highCD16+ monocytes. In the rat model of CPB, we further demonstrated that CPB induced migration of immature monocytes into the lungs, either from the bone marrow or from the spleen. Moreover, we confirmed the hypothesis that immature subsets could contribute to CPB-induced acute lung injury by giving rise to TNF-α producing descendants.
CONCLUSIONS: The immature CD14lowCD16- monocytes might contribute to blood-circuit contact-induced acute lung injury by generating TNF-α-producing, mature monocytes. New strategies based on monocyte manipulation could be a promising therapeutic approach for minimising CPB-related lung injury. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

Entities:  

Keywords:  ARDS; Innate Immunity; Macrophage Biology

Mesh:

Substances:

Year:  2016        PMID: 27660037     DOI: 10.1136/thoraxjnl-2015-208023

Source DB:  PubMed          Journal:  Thorax        ISSN: 0040-6376            Impact factor:   9.139


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  6 in total

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