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中华危重症医学杂志(电子版) ›› 2024, Vol. 17 ›› Issue (02) : 148 -154. doi: 10.3877/cma.j.issn.1674-6880.2024.02.011

综述

巨噬细胞程序性死亡在急性肺损伤/急性呼吸窘迫综合征中的研究进展
张丽敏1, 张志明1,(), 李兴芳1, 董敏1, 韩冰阁1, 颉志英2, 雍文兴2   
  1. 1. 730050 兰州,甘肃省中医院呼吸与危重症医学科
    2. 730000 兰州,甘肃中医药大学附属医院急诊科
  • 收稿日期:2023-02-14 出版日期:2024-04-30
  • 通信作者: 张志明
  • 基金资助:
    甘肃省重点课题项目(GZKP-2020-8); 兰州市人才创新创业专项(2021-RC-80)
  • Received:2023-02-14 Published:2024-04-30
引用本文:

张丽敏, 张志明, 李兴芳, 董敏, 韩冰阁, 颉志英, 雍文兴. 巨噬细胞程序性死亡在急性肺损伤/急性呼吸窘迫综合征中的研究进展[J]. 中华危重症医学杂志(电子版), 2024, 17(02): 148-154.

急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是一个破坏性的临床问题,具有较高的发病率和病死率。ALI/ARDS是世界范围内急危重症疾病难以克服的问题之一,常伴有多器官功能衰竭[1]。在临床上,ALI/ARDS主要表现为显著的低氧血症、弥漫性双肺浸润、肺水肿、肺顺应性降低以及功能性残余容量减少等[2]。ALI/ARDS的病理特点包括肺泡毛细血管膜功能障碍导致血管通透性增加、高蛋白液泛滥、肺泡出血和纤维蛋白沉积,其发病机制尚未完全阐明,主要涉及不受控制的炎症反应、水通道蛋白调控、凝血/纤溶系统失衡、凋亡、自噬、焦亡等细胞程序性死亡相关机制[3]。而在ALI/ARDS发生发展中特定的生物标志物提示特定类型的肺细胞包括肺泡上皮细胞、内皮细胞、巨噬细胞等的损伤或激活,且越来越多的证据表明巨噬细胞是ALI/ARDS发病的关键因素,因此确认巨噬细胞在ALI/ARDS中作用的细胞和分子机制将为一些潜在的治疗策略提供基础[4]

1
Mowery NT, Terzian WTH, Nelson AC. Acute lung injury[J]. Curr Probl Surg, 2020, 57 (5): 100777.
2
滕飞,贾玲玲,赵希伟,等.外泌体在急性肺损伤/急性呼吸窘迫综合征中的研究进展[J/CD].中华危重症医学杂志(电子版)202114(3):252-256.
3
Zhou H, Fan EK, Fan J. Cell-cell interaction mechanisms in acute lung injury[J]. Shock, 2021, 55 (2): 167-176.
4
Butt Y, Kurdowska A, Allen TC. Acute lung injury: a clinical and molecular review[J]. Arch Pathol Lab Med, 2016, 140 (4): 345-350.
5
Shapouri-Moghaddam A, Mohammadlan S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J]. J Cell Physiol, 2018, 233 (9): 6425-6440.
6
Artyomov MN, Sergushichev A, Schilling JD. Integrating immunometabolism and macrophage diversity[J]. Semin Immunol, 2016, 28 (5): 417-424.
7
Chorro L, Sarde A, Li M, et al. Langerhans cell (LC) proliferation mediates neonatal development, homeostasis, and inflammation-associated expansion of the epidermal LC network[J]. J Exp Med, 2009, 206 (13): 3089-3100.
8
Hume DA, Irvine KM, Pridans C. The mononuclear phagocyte system: the relationship between monocytes and macrophages[J]. Trends Immunol, 2019, 40 (2): 98-112.
9
Mu X, Li Y, Fan GC. Tissue-resident macrophages in the control of infection and resolution of inflammation[J]. Shock, 2021, 55 (1): 14-23.
10
Mass E, Ballesteros I, Farlik M, et al. Specification of tissue-resident macrophages during organogenesis[J]. Science, 2016, 353 (6304): aaf4238.
11
Lim PN, Cervantes MM, Pham LK, et al. Alveolar macrophages: novel therapeutic targets for respiratory diseases[J]. Expert Rev Mol Med, 2021 (23): e18.
12
Bissonnette EY, Lauzon-Joset JF, Debley JS, et al. Cross-talk between alveolar macrophages and lung epithelial cells is essential to maintain lung homeostasis[J]. Front Immunol, 2020 (11): 583042.
13
Schyns J, Bureau F, Marichal T. Lung interstitial macrophages: past, present, and future[J]. J Immunol Res, 2018 (2018): 5160794.
14
Gibbings SL, Thomas SM, Atif SM, et al. Three unique interstitial macrophages in the murine lung at steady state[J]. Am J Respir Cell Mol Biol, 2017, 57(1): 66-76.
15
Xing Z, Afkhami S, Bavananthasivam J, et al. Innate immune memory of tissue-resident macrophages and trained innate immunity: re-vamping vaccine concept and strategies[J]. J Leukoc Biol, 2020, 108 (3): 825-834.
16
Watanabe S, Alexander M, Misharin AV, et al. The role of macrophages in the resolution of inflammation[J]. J Clin Invest, 2019, 129 (7): 2619-2628.
17
Orecchioni M, Ghosheh Y, Pramod AB, et al. Macrophage polarization: different gene signatures in M1 (LPS+) vs. classically and M2 (LPS-) vs. alternatively activated macrophages[J]. Front Immunol, 2019 (10): 1084.
18
Bosco MC. Macrophage polarization: reaching across the aisle?[J]. J Allergy Clin Immunol, 2019, 143 (4): 1348-1350.
19
Zhang Y, Li X, Luo Z, et al. ECM1 is an essential factor for the determination of M1 macrophage polarization in IBD in response to LPS stimulation[J]. Proc Natl Acad Sci U S A, 2020, 117 (6): 3083-3092.
20
Zhang L, Wang Y, Wu G, et al. Macrophages: friend or foe in idiopathic pulmonary fibrosis?[J]. Respir Res, 2018, 19 (1): 170.
21
Dong R, Zhang B, Tan B, et al. Long non-coding RNAs as the regulators and targets of macrophage M2 polarization[J]. Life Sci, 2021 (266): 118895.
22
Wang Y, Smith W, Hao D, et al. M1 and M2 macrophage polarization and potentially therapeutic naturally occurring compounds[J]. Int Immunopharmacol, 2019 (70): 459-466.
23
Wang LX, Zhang SX, Wu HJ, et al. M2b macrophage polarization and its roles in diseases[J]. J Leukoc Biol, 2019, 106 (2): 345-358.
24
赵希伟,周佳伟,刘凯,等.连接蛋白43通过蛋白激酶A介导丝氨酸373调控脓毒症急性肺损伤肺泡Ⅱ型上皮细胞屏障功能的研究[J/CD].中华危重症医学杂志(电子版)202114(5):355-361.
25
Li Y, Huang J, Foley NM, et al. B7H3 ameliorates LPS-induced acute lung injury via attenuation of neutrophil migration and infiltration[J]. Sci Rep, 2016 (6): 31284.
26
Niu X, Zang L, Li W, et al. Anti-inflammatory effect of Yam Glycoprotein on lipopolysaccharide-induced acute lung injury via the NLRP3 and NF-κB/TLR4 signaling pathway[J]. Int Immunopharmacol, 2020 (81): 106024.
27
Li X, Huang R, Liu K, et al. Fucoxanthin attenuates LPS-induced acute lung injury via inhibition of the TLR4/MyD88 signaling axis[J]. Aging (Albany NY), 2020, 13 (2): 2655-2667.
28
Wang C, Ma C, Gong L, et al. Macrophage polarization and its role in liver disease[J]. Front Immunol, 2021 (12): 803037.
29
Chen X, Tang J, Shuai W, et al. Macrophage polarization and its role in the pathogenesis of acute lung injury/acute respiratory distress syndrome[J]. Inflamm Res, 2020, 69 (9): 883-895.
30
Bedoui S, Herold MJ, Strasser A. Emerging connectivity of programmed cell death pathways and its physiological implications[J]. Nat Rev Mol Cell Biol, 2020, 21 (11): 678-695.
31
Klionsky DJ, Petroni G, Amaravadi RK, et al. Autophagy in major human diseases[J]. EMBO J, 2021, 40 (19): e108863.
32
Münz C. The macroautophagy machinery in endo- and exocytosis[J]. J Mol Biol, 2017, 429 (4): 473-485.
33
Martin FP, Jacqueline C, Poschmann J, et al. Alveolar macrophages: adaptation to their anatomic niche during and after inflammation[J]. Cells, 2021, 10 (10): 2720.
34
Liu F, Nie C, Zhao N, et al. MiR-155 alleviates septic lung injury by inducing autophagy via inhibition of transforming growth factor-β-activated binding protein 2[J]. Shock, 2017, 48 (1): 61-68.
35
Liu H, Zhou K, Liao L, et al. Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling[J]. Respir Res, 2018, 19 (1): 243.
36
Qian Q, Cao X, Wang B, et al. Endoplasmic reticulum stress potentiates the autophagy of alveolar macrophage to attenuate acute lung injury and airway inflammation[J]. Cell Cycle, 2020, 19 (5): 567-576.
37
D'Arcy MS. Cell death: a review of the major forms of apoptosis, necrosis and autophagy[J]. Cell Biol Int, 2019, 43 (6): 582-592.
38
Noone PM, Reddy SP. Recent advances in dead cell clearance during acute lung injury and repair[J]. Fac Rev, 2021 (10): 33.
39
Janssen WJ, Barthel L, Muldrow A, et al. Fas determines differential fates of resident and recruited macrophages during resolution of acute lung injury[J]. Am J Respir Crit Care Med, 2011, 184 (5): 547-560.
40
Hu R, Chen ZF, Yan J, et al. Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis[J]. Cell Death Dis, 2014, 5 (7): e1330.
41
Zhang P, Yu WW, Peng J, et al. LukS-PV induces apoptosis in acute myeloid leukemia cells mediated by C5a receptor[J]. Cancer Med, 2019, 8 (5): 2474-2483.
42
Yang L, Zhang Z, Zhuo Y, et al. Resveratrol alleviates sepsis-induced acute lung injury by suppressing inflammation and apoptosis of alveolar macrophage cells[J]. Am J Transl Res, 2018, 10 (7): 1961-1975.
43
Habashi NM, Camporota L, Gatto LA, et al. Functional pathophysiology of SARS-CoV-2-induced acute lung injury and clinical implications[J]. J Appl Physiol (1985), 2021, 130 (3): 877-891.
44
Grant RA, Morales-Nebreda L, Markov NS, et al. Circuits between infected macrophages and T cells in SARS-CoV-2 pneumonia[J]. Nature, 2021, 590 (7847): 635-641.
45
Fang Y, Tian S, Pan Y, et al. Pyroptosis: a new frontier in cancer[J]. Biomed Pharmacother, 2020 (121): 109595.
46
Frank D, Vince JE. Pyroptosis versus necroptosis: similarities, differences, and crosstalk[J]. Cell Death Differ, 2019, 26 (1): 99-114.
47
Swanson KV, Deng M, Ting JP. The NLRP3 inflammasome: molecular activation and regulation to therapeutics[J]. Nat Rev Immunol, 2019, 19 (8): 477-489.
48
Ding H, Yang J, Chen L, et al. Memantine alleviates acute lung injury via inhibiting macrophage pyroptosis[J]. Shock, 2021, 56 (6): 1040-1048.
49
He X, Qian Y, Li Z, et al. TLR4-upregulated IL-1β and IL-1RI promote alveolar macrophage pyroptosis and lung inflammation through an autocrine mechanism[J]. Sci Rep, 2016 (6): 31663.
50
Wu D, Pan P, Su X, et al. Interferon regulatory factor-1 mediates alveolar macrophage pyroptosis during LPS-induced acute lung injury in mice[J]. Shock, 2016, 46 (3): 329-338.
51
Wei LY, Jiang AQ, Jiang R, et al. Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization[J]. Innate Immun, 2021, 27 (4): 313-323.
52
Jiao Y, Zhang T, Zhang C, et al. Exosomal miR-30d-5p of neutrophils induces M1 macrophage polarization and primes macrophage pyroptosis in sepsis-related acute lung injury[J]. Crit Care, 2021, 25 (1): 356.
53
Stockwell BR, Jiang X, Gu W. Emerging mechanisms and disease relevance of ferroptosis[J]. Trends Cell Biol, 2020, 30 (6): 478-490.
54
Hirschhorn T, Stockwell BR. The development of the concept of ferroptosis[J]. Free Radic Biol Med, 2019 (133): 130-143.
55
Zhou H, Li F, Niu JY, et al. Ferroptosis was involved in the oleic acid-induced acute lung injury in mice[J]. Sheng Li Xue Bao, 2019, 71 (5): 689-697.
56
Li Y, Cao Y, Xiao J, et al. Inhibitor of apoptosis-stimulating protein of p53 inhibits ferroptosis and alleviates intestinal ischemia/reperfusion-induced acute lung injury[J]. Cell Death Differ, 2020, 27 (9): 2635-2650.
57
Liu P, Feng Y, Li H, et al. Ferrostatin-1 alleviates lipopolysaccharide-induced acute lung injury via inhibiting ferroptosis[J]. Cell Mol Biol Lett, 2020 (25): 10.
58
Xu Y, Li X, Cheng Y, et al. Inhibition of ACSL4 attenuates ferroptotic damage after pulmonary ischemia-reperfusion[J]. FASEB J, 2020, 34 (12): 16262-16275.
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