巨噬细胞重编程参与巨噬细胞吞噬功能/死亡调节在脓毒症中的意义_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

胡纯娣 ,  李慧

中山大学附属第七医院呼吸与危重症医学科（深圳 518107）;

Corresponding author：

李慧, Email: lihui@sysush.com

Keywords：

DOI：

10.7507/1671-6205.202406092

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Citation： 胡纯娣, 李慧. 巨噬细胞重编程参与巨噬细胞吞噬功能/死亡调节在脓毒症中的意义. Chinese Journal of Respiratory and Critical Care Medicine, 2025, 24(5): 365-371. doi: 10.7507/1671-6205.202406092 Copy

1.	Im Y, Kang D, Ko R E, et al. Time-to-antibiotics and clinical outcomes in patients with sepsis and septic shock: a prospective nationwide multicenter cohort study. Crit Care, 2022, 26(1): 19.
2.	Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet, 2020, 395(10219): 200-211.
3.	La Via L, Sangiorgio G, Stefani S, et al. The Global Burden of Sepsis and Septic Shock. Epidemiologia (Basel), 2024, 5(3): 456-478.
4.	Chen X, Liu Y, Gao Y, et al. The roles of macrophage polarization in the host immune response to sepsis. Int Immunopharmacol, 2021, 96: 107791.
5.	Gordon S, Taylor PR. Monocyte and macrophage heterogeneity. Nat Rev Immunol, 2005, 5(12): 953-964.
6.	Kumar V. Targeting macrophage immunometabolism: dawn in the darkness of sepsis. Int Immunopharmacol, 2018, 58: 173-185.
7.	Wynn T A, Barron L. Macrophages: master regulators of inflammation and fibrosis. Semin Liver Dis, 2010, 30(3): 245-257.
8.	Roquilly A, Jacqueline C, Davieau M, et al. Alveolar macrophages are epigenetically altered after inflammation, leading to long-term lung immunoparalysis. Nat Immunol, 2020, 21(6): 636-648.
9.	Liu D, Huang S Y, Sun J H, et al. Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options. Mil Med Res, 2022, 9(1): 56.
10.	De Santa F, Totaro M G, Prosperini E, et al. The histone H3 lysine-27 demethylase Jmjd3 links inflammation to inhibition of polycomb-mediated gene silencing. Cell, 2007, 130(6): 1083-1094.
11.	Deng M, Tang Y, Li W, et al. The endotoxin delivery protein HMGB1 mediates caspase-11-dependent lethality in sepsis. Immunity, 2018, 49(4): 740-753,e7.
12.	Delano MJ, Ward PA. The immune system's role in sepsis progression, resolution, and long-term outcome. Immunol Rev, 2016, 274(1): 330-353.
13.	Luan YY, Dong N, Xie M, et al. The significance and regulatory mechanisms of innate immune cells in the development of sepsis. J Interferon Cytokine Res, 2014, 34(1): 2-15.
14.	Epelman S, Lavine KJ, Randolph GJ. Origin and functions of tissue macrophages. Immunity, 2014, 41(1): 21-35.
15.	Gordon S, Plüddemann A. Tissue macrophages: heterogeneity and functions. BMC Biol, 2017, 15(1): 53.
16.	Feng A, Ao X, Zhou N, et al. A novel risk-prediction scoring system for sepsis among patients with acute pancreatitis: a retrospective analysis of a large clinical database. Int J Clin Pract, 2022, 2022: 5435656.
17.	Sun JK, Nie S, Chen YM, et al. Effects of permissive hypocaloric vs standard enteral feeding on gastrointestinal function and outcomes in sepsis. World J Gastroenterol, 2021, 27(29): 4900-4912.
18.	Lauvau G, Loke P, Hohl TM. Monocyte-mediated defense against bacteria, fungi, and parasites. Semin Immunol, 2015, 27(6): 397-409.
19.	Hamidzadeh K, Christensen S M, Dalby E, et al. Macrophages and the recovery from acute and chronic inflammation. Annu Rev Physiol, 2017, 79: 567-592.
20.	Gao YL, Yao Y, Zhang X, et al. Regulatory T cells: angels or demons in the pathophysiology of sepsis?. Front Immunol, 2022, 13: 829210.
21.	Wang TS, Deng JC. Molecular and cellular aspects of sepsis-induced immunosuppression. J Mol Med (Berl), 2008, 86(5): 495-506.
22.	Winkler MS, Rissiek A, Priefler M, et al. Human leucocyte antigen (HLA-DR) gene expression is reduced in sepsis and correlates with impaired TNFα response: A diagnostic tool for immunosuppression?. PLoS One, 2017, 12(8): e0182427.
23.	Shin DM, Yang CS, Yuk JM, et al. Mycobacterium abscessus activates the macrophage innate immune response via a physical and functional interaction between TLR2 and dectin-1. Cell Microbiol, 2008, 10(8): 1608-1621.
24.	Hiruma T, Tsuyuzaki H, Uchida K, et al. IFN-β improves sepsis-related alveolar macrophage dysfunction and postseptic acute respiratory distress syndrome-related mortality. Am J Respir Cell Mol Biol, 2018, 59(1): 45-55.
25.	Körner A, Bernard A, Fitzgerald J C, et al. Sema7A is crucial for resolution of severe inflammation. Proc Natl Acad Sci U S A, 2021, 118(9): e2017527118.
26.	Choi S, Kim T. Compound K - an immunomodulator of macrophages in inflammation. Life Sci, 2023, 323: 121700.
27.	Meyers AK, Wang Z, Han W, et al. Pyruvate dehydrogenase kinase supports macrophage NLRP3 inflammasome activation during acute inflammation. Cell Rep, 2023, 42(1): 111941.
28.	Bauer M, Wetzker R. The cellular basis of organ failure in sepsis-signaling during damage and repair processes. Med Klin Intensivmed Notfmed, 2020, 115(Suppl 1): 4-9.
29.	Ni P, Liu YQ, Man JY, et al. C16, a novel sinomenine derivatives, promoted macrophage reprogramming toward M2-like phenotype and protected mice from endotoxemia. Int J Immunopathol Pharmacol, 2021, 35: 20587384211026786.
30.	Mills EL, Kelly B, O'neill LAJ. Mitochondria are the powerhouses of immunity. Nat Immunol, 2017, 18(5): 488-498.
31.	Monlun M, Hyernard C, Blanco P, et al. Mitochondria as molecular platforms integrating multiple innate immune signalings. J Mol Biol, 2017, 429(1): 1-13.
32.	Mikkelsen ME, Miltiades AN, Gaieski DF, et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Crit Care Med, 2009, 37(5): 1670-1677.
33.	Wang Z, Kong L, Tan S, et al. Zhx2 Accelerates sepsis by promoting macrophage glycolysis via Pfkfb3. J Immunol, 2020, 204(8): 2232-2241.
34.	Lu XJ, Chen J, Yu CH, et al. LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor. J Exp Med, 2013, 210(1): 5-13.
35.	Xia H, Chen L, Liu H, et al. Protectin DX increases survival in a mouse model of sepsis by ameliorating inflammation and modulating macrophage phenotype. Sci Rep, 2017, 7(1): 99.
36.	Bohaud C, Johansen M D, Jorgensen C, et al. The role of macrophages during mammalian tissue remodeling and regeneration under infectious and non-infectious conditions. Front Immunol, 2021, 12: 707856.
37.	Mosser DM, Hamidzadeh K, Goncalves R. Macrophages and the maintenance of homeostasis. Cell Mol Immunol, 2021, 18(3): 579-587.
38.	Jiang W, Le J, Wang P Y, et al. Extracellular acidity reprograms macrophage metabolism and innate responsiveness. J Immunol, 2021, 206(12): 3021-3031.
39.	王历, 张平安. 巨噬细胞糖代谢重编程在脓毒症中的研究进展. 微循环学杂志, 2023, 33(1): 108-112.
40.	Luo R, Li X, Wang D. Reprogramming macrophage metabolism and its effect on NLRP3 inflammasome activation in sepsis. Front Mol Biosci, 2022, 9: 917818.
41.	Liu W, Liu T, Zheng Y, et al. Metabolic reprogramming and its regulatory mechanism in sepsis-mediated inflammation. J Inflamm Res, 2023, 16: 1195-1207.
42.	Stincone A, Prigione A, Cramer T, et al. The return of metabolism: biochemistry and physiology of the pentose phosphate pathway. Biol Rev Camb Philos Soc, 2015, 90(3): 927-963.
43.	Bone RC, Grodzin CJ, Balk RA. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest, 1997, 112(1): 235-243.
44.	Hotchkiss RS, Monneret G, Payen D. Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Nat Rev Immunol, 2013, 13(12): 862-874.
45.	Venet F, Monneret G. Advances in the understanding and treatment of sepsis-induced immunosuppression. Nat Rev Nephrol, 2018, 14(2): 121-137.
46.	Cartier A, Hla T. Sphingosine 1-phosphate: Lipid signaling in pathology and therapy. Science, 2019, 366(6463).
47.	Song F, Hou J, Chen Z, et al. Sphingosine-1-phosphate receptor 2 signaling promotes caspase-11-dependent macrophage pyroptosis and worsens Escherichia coli sepsis outcome. Anesthesiology, 2018, 129(2): 311-320.
48.	Hou J, Chen Q, Zhang K, et al. Sphingosine 1-phosphate receptor 2 signaling suppresses macrophage phagocytosis and impairs host defense against sepsis. Anesthesiology, 2015, 123(2): 409-422.
49.	Fang C, Ren P, Bian G, et al. Enhancing Spns2/S1P in macrophages alleviates hyperinflammation and prevents immunosuppression in sepsis. EMBO Rep, 2023, 24(8): e56635.
50.	Hotchkiss RS, Monneret G, Payen D. Immunosuppression in sepsis: a novel understanding of the disorder and a new therapeutic approach. Lancet Infect Dis, 2013, 13(3): 260-268.
51.	Dominguez-Andres J, Netea MG. Long-term reprogramming of the innate immune system. J Leukoc Biol, 2019, 105(2): 329-338.
52.	Riedemann NC, Guo RF, Ward PA. Novel strategies for the treatment of sepsis. Nat Med, 2003, 9(5): 517-524.
53.	Santos SS, Carmo AM, Brunialti MK, et al. Modulation of monocytes in septic patients: preserved phagocytic activity, increased ROS and NO generation, and decreased production of inflammatory cytokines. Intensive Care Med Exp, 2016, 4(1): 5.
54.	Shalova IN, Lim JY, Chittezhath M, et al. Human monocytes undergo functional re-programming during sepsis mediated by hypoxia-inducible factor-1α. Immunity, 2015, 42(3): 484-98.
55.	Lachmandas E, Beigier-Bompadre M, Cheng SC, et al. Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells. Eur J Immunol, 2016, 46(11): 2574-2586.
56.	Escoll P, Buchrieser C. Metabolic reprogramming: an innate cellular defence mechanism against intracellular bacteria?. Curr Opin Immunol, 2019, 60: 117-123.
57.	Li H, Luo YF, Wang YS, et al. Using ROS as a second messenger, NADPH oxidase 2 mediates macrophage senescence via interaction with NF-κB during Pseudomonas aeruginosa infection. Oxid Med Cell Longev, 2018, 2018: 9741838.
58.	Li H, Luo YF, Wang YS, et al. Pseudomonas aeruginosa induces cellular senescence in lung tissue at the early stage of two-hit septic mice. Pathog Dis, 2018, 76(9).
59.	Zhao Q, Luo Y F, Tian M, et al. Activating transcription factor 3 involved in Pseudomonas aeruginosa PAO1-induced macrophage senescence. Mol Immunol, 2021, 133: 122-127.
60.	Wolk K, Döcke WD, Von Baehr V, et al. Impaired antigen presentation by human monocytes during endotoxin tolerance. Blood, 2000, 96(1): 218-223.
61.	Hou J, Chen Q, Wu X, et al. S1PR3 Signaling drives bacterial killing and is required for survival in bacterial sepsis. Am J Respir Crit Care Med, 2017, 196(12): 1559-1570.
62.	Aachoui Y, Leaf I A, Hagar J A, et al. Caspase-11 protects against bacteria that escape the vacuole. Science, 2013, 339(6122): 975-978.
63.	Broz P, Ruby T, Belhocine K, et al. Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Nature, 2012, 490(7419): 288-291.
64.	Hagar JA, Powell DA, Aachoui Y, et al. Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock. Science, 2013, 341(6151): 1250-1253.
65.	Kayagaki N, Warming S, Lamkanfi M, et al. Non-canonical inflammasome activation targets caspase-11. Nature, 2011, 479(7371): 117-121.
66.	Kayagaki N, Wong MT, Stowe IB, et al. Noncanonical inflammasome activation by intracellular LPS independent of TLR4. Science, 2013, 341(6151): 1246-1249.
67.	Rathinam VA, Vanaja SK, Waggoner L, et al. TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria. Cell, 2012, 150(3): 606-619.
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1. Im Y, Kang D, Ko R E, et al. Time-to-antibiotics and clinical outcomes in patients with sepsis and septic shock: a prospective nationwide multicenter cohort study. Crit Care, 2022, 26(1): 19.
2. Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet, 2020, 395(10219): 200-211.
3. La Via L, Sangiorgio G, Stefani S, et al. The Global Burden of Sepsis and Septic Shock. Epidemiologia (Basel), 2024, 5(3): 456-478.
4. Chen X, Liu Y, Gao Y, et al. The roles of macrophage polarization in the host immune response to sepsis. Int Immunopharmacol, 2021, 96: 107791.
5. Gordon S, Taylor PR. Monocyte and macrophage heterogeneity. Nat Rev Immunol, 2005, 5(12): 953-964.
6. Kumar V. Targeting macrophage immunometabolism: dawn in the darkness of sepsis. Int Immunopharmacol, 2018, 58: 173-185.
7. Wynn T A, Barron L. Macrophages: master regulators of inflammation and fibrosis. Semin Liver Dis, 2010, 30(3): 245-257.
8. Roquilly A, Jacqueline C, Davieau M, et al. Alveolar macrophages are epigenetically altered after inflammation, leading to long-term lung immunoparalysis. Nat Immunol, 2020, 21(6): 636-648.
9. Liu D, Huang S Y, Sun J H, et al. Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options. Mil Med Res, 2022, 9(1): 56.
10. De Santa F, Totaro M G, Prosperini E, et al. The histone H3 lysine-27 demethylase Jmjd3 links inflammation to inhibition of polycomb-mediated gene silencing. Cell, 2007, 130(6): 1083-1094.
11. Deng M, Tang Y, Li W, et al. The endotoxin delivery protein HMGB1 mediates caspase-11-dependent lethality in sepsis. Immunity, 2018, 49(4): 740-753,e7.
12. Delano MJ, Ward PA. The immune system's role in sepsis progression, resolution, and long-term outcome. Immunol Rev, 2016, 274(1): 330-353.
13. Luan YY, Dong N, Xie M, et al. The significance and regulatory mechanisms of innate immune cells in the development of sepsis. J Interferon Cytokine Res, 2014, 34(1): 2-15.
14. Epelman S, Lavine KJ, Randolph GJ. Origin and functions of tissue macrophages. Immunity, 2014, 41(1): 21-35.
15. Gordon S, Plüddemann A. Tissue macrophages: heterogeneity and functions. BMC Biol, 2017, 15(1): 53.
16. Feng A, Ao X, Zhou N, et al. A novel risk-prediction scoring system for sepsis among patients with acute pancreatitis: a retrospective analysis of a large clinical database. Int J Clin Pract, 2022, 2022: 5435656.
17. Sun JK, Nie S, Chen YM, et al. Effects of permissive hypocaloric vs standard enteral feeding on gastrointestinal function and outcomes in sepsis. World J Gastroenterol, 2021, 27(29): 4900-4912.
18. Lauvau G, Loke P, Hohl TM. Monocyte-mediated defense against bacteria, fungi, and parasites. Semin Immunol, 2015, 27(6): 397-409.
19. Hamidzadeh K, Christensen S M, Dalby E, et al. Macrophages and the recovery from acute and chronic inflammation. Annu Rev Physiol, 2017, 79: 567-592.
20. Gao YL, Yao Y, Zhang X, et al. Regulatory T cells: angels or demons in the pathophysiology of sepsis?. Front Immunol, 2022, 13: 829210.
21. Wang TS, Deng JC. Molecular and cellular aspects of sepsis-induced immunosuppression. J Mol Med (Berl), 2008, 86(5): 495-506.
22. Winkler MS, Rissiek A, Priefler M, et al. Human leucocyte antigen (HLA-DR) gene expression is reduced in sepsis and correlates with impaired TNFα response: A diagnostic tool for immunosuppression?. PLoS One, 2017, 12(8): e0182427.
23. Shin DM, Yang CS, Yuk JM, et al. Mycobacterium abscessus activates the macrophage innate immune response via a physical and functional interaction between TLR2 and dectin-1. Cell Microbiol, 2008, 10(8): 1608-1621.
24. Hiruma T, Tsuyuzaki H, Uchida K, et al. IFN-β improves sepsis-related alveolar macrophage dysfunction and postseptic acute respiratory distress syndrome-related mortality. Am J Respir Cell Mol Biol, 2018, 59(1): 45-55.
25. Körner A, Bernard A, Fitzgerald J C, et al. Sema7A is crucial for resolution of severe inflammation. Proc Natl Acad Sci U S A, 2021, 118(9): e2017527118.
26. Choi S, Kim T. Compound K - an immunomodulator of macrophages in inflammation. Life Sci, 2023, 323: 121700.
27. Meyers AK, Wang Z, Han W, et al. Pyruvate dehydrogenase kinase supports macrophage NLRP3 inflammasome activation during acute inflammation. Cell Rep, 2023, 42(1): 111941.
28. Bauer M, Wetzker R. The cellular basis of organ failure in sepsis-signaling during damage and repair processes. Med Klin Intensivmed Notfmed, 2020, 115(Suppl 1): 4-9.
29. Ni P, Liu YQ, Man JY, et al. C16, a novel sinomenine derivatives, promoted macrophage reprogramming toward M2-like phenotype and protected mice from endotoxemia. Int J Immunopathol Pharmacol, 2021, 35: 20587384211026786.
30. Mills EL, Kelly B, O'neill LAJ. Mitochondria are the powerhouses of immunity. Nat Immunol, 2017, 18(5): 488-498.
31. Monlun M, Hyernard C, Blanco P, et al. Mitochondria as molecular platforms integrating multiple innate immune signalings. J Mol Biol, 2017, 429(1): 1-13.
32. Mikkelsen ME, Miltiades AN, Gaieski DF, et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Crit Care Med, 2009, 37(5): 1670-1677.
33. Wang Z, Kong L, Tan S, et al. Zhx2 Accelerates sepsis by promoting macrophage glycolysis via Pfkfb3. J Immunol, 2020, 204(8): 2232-2241.
34. Lu XJ, Chen J, Yu CH, et al. LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor. J Exp Med, 2013, 210(1): 5-13.
35. Xia H, Chen L, Liu H, et al. Protectin DX increases survival in a mouse model of sepsis by ameliorating inflammation and modulating macrophage phenotype. Sci Rep, 2017, 7(1): 99.
36. Bohaud C, Johansen M D, Jorgensen C, et al. The role of macrophages during mammalian tissue remodeling and regeneration under infectious and non-infectious conditions. Front Immunol, 2021, 12: 707856.
37. Mosser DM, Hamidzadeh K, Goncalves R. Macrophages and the maintenance of homeostasis. Cell Mol Immunol, 2021, 18(3): 579-587.
38. Jiang W, Le J, Wang P Y, et al. Extracellular acidity reprograms macrophage metabolism and innate responsiveness. J Immunol, 2021, 206(12): 3021-3031.
39. 王历, 张平安. 巨噬细胞糖代谢重编程在脓毒症中的研究进展. 微循环学杂志, 2023, 33(1): 108-112.
40. Luo R, Li X, Wang D. Reprogramming macrophage metabolism and its effect on NLRP3 inflammasome activation in sepsis. Front Mol Biosci, 2022, 9: 917818.
41. Liu W, Liu T, Zheng Y, et al. Metabolic reprogramming and its regulatory mechanism in sepsis-mediated inflammation. J Inflamm Res, 2023, 16: 1195-1207.
42. Stincone A, Prigione A, Cramer T, et al. The return of metabolism: biochemistry and physiology of the pentose phosphate pathway. Biol Rev Camb Philos Soc, 2015, 90(3): 927-963.
43. Bone RC, Grodzin CJ, Balk RA. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest, 1997, 112(1): 235-243.
44. Hotchkiss RS, Monneret G, Payen D. Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Nat Rev Immunol, 2013, 13(12): 862-874.
45. Venet F, Monneret G. Advances in the understanding and treatment of sepsis-induced immunosuppression. Nat Rev Nephrol, 2018, 14(2): 121-137.
46. Cartier A, Hla T. Sphingosine 1-phosphate: Lipid signaling in pathology and therapy. Science, 2019, 366(6463).
47. Song F, Hou J, Chen Z, et al. Sphingosine-1-phosphate receptor 2 signaling promotes caspase-11-dependent macrophage pyroptosis and worsens Escherichia coli sepsis outcome. Anesthesiology, 2018, 129(2): 311-320.
48. Hou J, Chen Q, Zhang K, et al. Sphingosine 1-phosphate receptor 2 signaling suppresses macrophage phagocytosis and impairs host defense against sepsis. Anesthesiology, 2015, 123(2): 409-422.
49. Fang C, Ren P, Bian G, et al. Enhancing Spns2/S1P in macrophages alleviates hyperinflammation and prevents immunosuppression in sepsis. EMBO Rep, 2023, 24(8): e56635.
50. Hotchkiss RS, Monneret G, Payen D. Immunosuppression in sepsis: a novel understanding of the disorder and a new therapeutic approach. Lancet Infect Dis, 2013, 13(3): 260-268.
51. Dominguez-Andres J, Netea MG. Long-term reprogramming of the innate immune system. J Leukoc Biol, 2019, 105(2): 329-338.
52. Riedemann NC, Guo RF, Ward PA. Novel strategies for the treatment of sepsis. Nat Med, 2003, 9(5): 517-524.
53. Santos SS, Carmo AM, Brunialti MK, et al. Modulation of monocytes in septic patients: preserved phagocytic activity, increased ROS and NO generation, and decreased production of inflammatory cytokines. Intensive Care Med Exp, 2016, 4(1): 5.
54. Shalova IN, Lim JY, Chittezhath M, et al. Human monocytes undergo functional re-programming during sepsis mediated by hypoxia-inducible factor-1α. Immunity, 2015, 42(3): 484-98.
55. Lachmandas E, Beigier-Bompadre M, Cheng SC, et al. Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells. Eur J Immunol, 2016, 46(11): 2574-2586.
56. Escoll P, Buchrieser C. Metabolic reprogramming: an innate cellular defence mechanism against intracellular bacteria?. Curr Opin Immunol, 2019, 60: 117-123.
57. Li H, Luo YF, Wang YS, et al. Using ROS as a second messenger, NADPH oxidase 2 mediates macrophage senescence via interaction with NF-κB during Pseudomonas aeruginosa infection. Oxid Med Cell Longev, 2018, 2018: 9741838.
58. Li H, Luo YF, Wang YS, et al. Pseudomonas aeruginosa induces cellular senescence in lung tissue at the early stage of two-hit septic mice. Pathog Dis, 2018, 76(9).
59. Zhao Q, Luo Y F, Tian M, et al. Activating transcription factor 3 involved in Pseudomonas aeruginosa PAO1-induced macrophage senescence. Mol Immunol, 2021, 133: 122-127.
60. Wolk K, Döcke WD, Von Baehr V, et al. Impaired antigen presentation by human monocytes during endotoxin tolerance. Blood, 2000, 96(1): 218-223.
61. Hou J, Chen Q, Wu X, et al. S1PR3 Signaling drives bacterial killing and is required for survival in bacterial sepsis. Am J Respir Crit Care Med, 2017, 196(12): 1559-1570.
62. Aachoui Y, Leaf I A, Hagar J A, et al. Caspase-11 protects against bacteria that escape the vacuole. Science, 2013, 339(6122): 975-978.
63. Broz P, Ruby T, Belhocine K, et al. Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Nature, 2012, 490(7419): 288-291.
64. Hagar JA, Powell DA, Aachoui Y, et al. Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock. Science, 2013, 341(6151): 1250-1253.
65. Kayagaki N, Warming S, Lamkanfi M, et al. Non-canonical inflammasome activation targets caspase-11. Nature, 2011, 479(7371): 117-121.
66. Kayagaki N, Wong MT, Stowe IB, et al. Noncanonical inflammasome activation by intracellular LPS independent of TLR4. Science, 2013, 341(6151): 1246-1249.
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Chinese Journal of Respiratory and Critical Care Medicine

巨噬细胞重编程参与巨噬细胞吞噬功能/死亡调节在脓毒症中的意义

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