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

Xing, Zhichen; Han, Junyan; Hao, Xing; Wang, Jinhong; Jiang, Chunjing; Yu, Honggang; Wang, Hong; Wu, Xueying; Shen, Liwei; Dong, Xiaorong; Li, Tong; Li, Guoli; Zhang, Jianping; Hou, Xiaotong; Zeng, Hui

doi:10.1136/thoraxjnl-2015-208023

Cited by 24 publications

(23 citation statements)

References 38 publications

(40 reference statements)

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“…T-lymphocytes were shown to be activated during CPB and to induce pulmonary damage [ 32 ]. Our CPB group showed elevated plasma concentrations of cytokines of both Th1 (e.g.…”

Section: Discussionmentioning

confidence: 99%

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

et al. 2018

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Cardiopulmonary bypass (CPB) with moderate hypothermic cardiac arrest (MHCA) is essential for prolonged complex procedures in cardiac surgery and is associated with postoperative complications. Although cytokine release provoked through MHCA under CPB plays a pivotal role in postoperative organ damage, the pathomechanisms are unclear. Here, we investigated the cytokine release pattern and histological organ damage after MHCA using a recently described mouse CPB model. Eight BALB/c mice underwent 60 minutes of circulatory arrest under CPB, were successively rewarmed and reperfused. Blood cytokine concentrations and liver and kidney function parameters were measured and histological changes to these organs were compared to control animals. Our results showed a marked increase in proinflammatory cytokines and histological changes in the kidney, lung, and liver after CPB. Furthermore, clinical chemistry showed signs of hemolysis and acute kidney injury. These results suggest early onset of solid organ injury which correlates with increased leukocyte infiltration. A better understanding of the interplay between pro-inflammatory cytokine activation and solid organ injury in this model of CBP with MHCA will inform strategies to reduce organ damage during cardiac surgeries in the clinic.

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“…T-lymphocytes were shown to be activated during CPB and to induce pulmonary damage [ 32 ]. Our CPB group showed elevated plasma concentrations of cytokines of both Th1 (e.g.…”

Section: Discussionmentioning

confidence: 99%

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

et al. 2018

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“…27 In the current study, we observed that prophylactic administration of methylprednisolone did not affect the percentage of immature Mo0 subsets which migrated into the peripheral blood from the bone marrow and spleen. 17 In addition, we found that methylprednisolone prophylaxis did not affect the percentage of inflammatory Mo2 subsets nor did it affect the expression levels of HLA-DR, CD86, CD64 and TLR-4 of each monocyte subset.…”

Section: Discussionmentioning

confidence: 62%

“…Next, we divided circulating monocytes into 4 subpopulations: CD14 low CD16 - (Mo0), CD14 high CD16 - (Mo1), CD14 high CD16 + (Mo2) and CD14 low CD16 + (Mo3) (Figure 2A). 17 The percentage of immature Mo0 monocytes rapidly increased during the CPB process, then returned to the normal range within 5 days post operation; following a slight decrease during CPB, inflammatory Mo2 monocyte subsets rapidly increased in the peripheral blood after CPB. Nevertheless, methylprednisolone did not significantly change the percentages (Figure 2B-E) and numbers of monocyte subsets (Figure 3A-D) in patients undergoing CPB.…”

Section: Resultsmentioning

confidence: 92%

The effect of methylprednisolone prophylaxis on inflammatory monocyte subsets and suppressive regulatory T cells of patients undergoing cardiopulmonary bypass

et al. 2019

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Background: Cardiopulmonary bypass (CPB) during open-heart surgery triggers an inflammatory response that can cause significant morbidity and mortality. Human monocytes and regulatory T (Treg) cells are phenotypically and functionally heterogeneous and have been shown to play a significant role in the inflammatory dysfunction triggered by CPB. Glucocorticoids (GCs) have been widely administered for decades in patients undergoing CPB to reduce this inflammatory response. However, it has not been clearly established how routine prophylactic administration of glucocorticoids (GCs) affects monocyte and Treg subsets. Methods: Thirty-six patient who underwent heart surgery with CPB were randomly assigned to a methylprednisolone group (MG, N = 18; 500 mg in the CPB priming) and a non-methylprednisolone group (NMG, N = 18). The circulating monocyte and Treg subsets were analyzed by flow cytometry. Results: The MG and NMG groups had comparable percentages of monocyte subsets and similar expression levels of HLA-DR, CD86, CD64 and toll-like receptor 4 (TLR4). Remarkably, methylprednisolone increased the percentage of CD4+CD25+ Treg cells among CD4+ T cells in patients undergoing CPB, but did not increase the proportion of suppressive Treg cells, either resting or activated, in these patients undergoing CPB. Conclusions: Our results showed that prophylactic administration of methylprednisolone neither decreased the percentages and counts of inflammatory monocyte subsets nor did it induce the expansion of suppressive Treg cells in patients undergoing CPB. These results clarified the effects of GCs on cell-mediated immune responses and provided additional evidence in practice. Trial registration: Clinicaltrials.gov : NCT01296074. Registered 14 February 2011.

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“…The mechanism of CPB-induced lung injury has not been fully elucidated, which is affected by many factors. At present, CPB-induced lung injury is mainly related to CPB-induced systemic inflammatory response syndrome (SIRS), lung ischemia/reperfusion (IR) injury, and respiratory mechanical ventilation [ 1 , 2 ]. Pulmonary arterial perfusion (PAP) with hypothermic protective solution (HPS) is one of the measures to reduce lung IR injury.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of HTK solution on postoperative pulmonary function in infants with CHD and PAH

Tian

et al. 2017

Bioscience Reports

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Objective: In the present study, we aimed to investigate the effect of pulmonary arterial perfusion (PAP) with Histidine–tryptophan–ketoglutarate (HTK) on lung protection in infants with congenital heart disease (CHD) and pulmonary arterial hypertension (PAH) after cardiopulmonary bypass (CPB).Methods: Fifty infant patients with CHD and PAH at our hospital from January, 2016 to February, 2017 were randomly divided into control group and HTK group. The levels of interleukin-6 (IL-6), malondialdehyde (MDA), and endothelin-1 (ET-1) in serum were detected using ELISA Kit. Oxygen index (OI) and respiratory index (RI) were calculated at each time point. The time of postoperative mechanical ventilation and ICU stay was counted, and the right lower lung tissues in patients were taken for pathological examination.Results: Compared with preanesthesia, the levels of IL-6, MDA, and ET-1 in the two groups were significantly increased after CPB, and their levels in HTK group were significantly lower than that in control group. Moreover, OI in control group decreased markedly and RI in control group increased significantly after CPB. Compared with control group, the postoperative mechanical ventilation time, postoperative ICU stay, and total hospital stay in HTK group were markedly short. In addition, inflammatory cells infiltration decreased and pulmonary interstitial showed mild edema in HTK group.Conclusion: PAP with HTK could effectively reduce CPB-induced lung injury and improve lung function.

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

Abstract: The immature CD14CD16 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.

Cited by 24 publications

References 38 publications

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

The effect of methylprednisolone prophylaxis on inflammatory monocyte subsets and suppressive regulatory T cells of patients undergoing cardiopulmonary bypass

Protective effect of HTK solution on postoperative pulmonary function in infants with CHD and PAH

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