Targeting the proinflammatory cytokine tumor necrosis factor-α to alleviate cardiopulmonary bypass-induced lung injury (Review)

Gao,Mingxin; Xie,Baodong; Gu,Chengxiong; Li,Haitao; Zhang,Fan; Yu,Yang

doi:10.3892/mmr.2014.3050

April-2015 Volume 11 Issue 4

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April-2015 Volume 11 Issue 4

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Review

Targeting the proinflammatory cytokine tumor necrosis factor-α to alleviate cardiopulmonary bypass-induced lung injury (Review)

Authors:
- Mingxin Gao
- Baodong Xie
- Chengxiong Gu
- Haitao Li
- Fan Zhang
- Yang Yu
View Affiliations / Copyright

Affiliations: Department of Cardiac Surgery, Beijing An Zhen Hospital, Capital Medical University, Beijing 100029, P.R. China, Department of Cardiovascular Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China
Pages: 2373-2378
|
Published online on: December 4, 2014

https://doi.org/10.3892/mmr.2014.3050
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Abstract

Pulmonary dysfunction is one of the most frequent complications associated with cardiopulmonary bypass (CPB). Multiple factors, including the contact of blood with the artificial surface of the CPB circuit, ischemia‑reperfusion and lung ventilator arrest elicit inflammatory reactions, consequently resulting in CPB‑induced lung injury. The proinflammatory cytokine tumor necrosis factor‑α (TNF‑α) has been demonstrated to have a critical role in mediating CPB‑induced pulmonary inflammation. The present review evaluated previous studies and summarized the effects of CPB on TNF‑α level in the serum and lung tissue of patients and animal models of CPB, the underlying mechanism of TNF‑α‑mediated lung injury and the therapeutic strategies for the inhibition of TNF‑α activity and production to attenuate CPB‑induced lung injury. TNF‑α level in the serum and lung tissue is significantly increased during and following CPB. TNF‑α mediates CPB‑induced lung damage by directly inducing apoptosis in alveolar epithelial cells and lung endothelial cells and by indirectly modulating the function of immune cells, including monocytes and macrophages. A functional neutralizing antibody to TNF‑α can reduce pulmonary TNF‑α production and attenuate CPB‑induced lung injury in a rabbit model of CPB. Inhibition of TNF‑α function and production using a neutralizing antibody to TNF‑α appears to be a promising therapeutic strategy to alleviate CPB‑induced lung injury.

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