Causality between 91 circulating inflammatory proteins and respiratory infections: a bidirectional Mendelian randomization study_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

ZHANG Lai ¹ ,  ZHANG Xiuying ² , ZHANG Shiyao ¹ , WEI Chenhao ¹ , LI Zhaoyang ¹

1. Liaoning University of Traditional Chinese Medicine, First Clinical College Shenyang, Shenyang, Liaoning 116600, P. R. China;
2. Department of Pediatrics, First Affiliated Hospital of Liaoning University of Chinese Medicine, Shenyang, Liaoning 110000, P. R. China;

Corresponding author：

ZHANG Xiuying, Email: pcxtcm@163.com

Keywords：

Respiratory infection; Mendelian randomization; inflammatory protein; acute laryngitis and bronchitis; acute bronchitis; acute bronchiolitis

DOI：

10.7507/1671-6205.202406074

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To investigate the causal relationship between 91 circulating inflammatory proteins and respiratory tract infection by bidirectional Mendelian randomization. Methods single nucleotide polymorphisms (SNPs) for 91 inflammatory circulating proteins were derived from GWAS data from a genome-wide association study of 14 824 subjects of European ancestry on the Olink Target platform, and SNPs for acute bronchitis, acute bronchiolitis, and acute laryngitis and tracheitis were derived from GWAS pooled data in the FinnGen database. Inverse variance weighting method was used as the main research method to conduct bidirectional Mendelian randomization analysis, and Cochran’ IVW Q test, MR-Egger regression method and one by one elimination method were used to conduct sensitivity tests to evaluate heterogeneity and horizontal pleiotropy. In order to reduce the incidence of Class I errors and improve the feasibility of the study, Bonferroni correction was performed.Results Levels of C hemokine C-X-C motif ligand 6 (CXCL6), matrix metalloproteinase-1 (MMP-1), hepatocyte growth factor (HGF), interleukin-10 (IL-10), chemokine C-X3-C motif ligand 1 (CX3CL1), and TNF-related activation-induced cytokine (TRANCE) were causally associated with acute bronchitis. MMP-1 level [OR: 1.239 0, 95%CI: 1.111 6-1.382 2, P<0.000 5] had a significant causal relationship with acute bronchitiss and played a promoting role. Levels of macrophage inflammatory protein-1α (MIP-1α), signaling lymphocyte activating molecules, and FMS-associated tyrosine kinase 3 ligand (FIt3L) were potentially causally associated with acute bronchiolitis. There was a potential causal relationship between C-X-C motif chemokine 5 (CXCL5), T cell surface glycoprotein CD6 subtype (CD6), fibroblast growth factor 19 (FGF-19), C-C motif chemokine 23 (CCL23), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor ligand superfamily member 12 (TNFSF12) levels and acute laryngitis and tracheitis. In reverse Mendelian randomization analysis, there were no positive results between acute bronchitis, acute bronchiolitis and 91 inflammatory factors. Acute laryngitis and tracheitis [OR: 1.076 3,95%CI: 1.012 9-1.143 7, P=0.017 6] were potentially causally associated with FGF-19 levels. Conclusions MMP-1 level have a significant causal relationship with acute bronchitis. The levels of other inflammatory factors such as CXCL6, HGF, MIP-1 alpha, FIt3L, CXCL5, FGF-19 are potentially causally associated with respiratory tract infections. MMP-1 may be an important target for the prediction or treatment of acute bronchitis.

Citation： ZHANG Lai, ZHANG Xiuying, ZHANG Shiyao, WEI Chenhao, LI Zhaoyang. Causality between 91 circulating inflammatory proteins and respiratory infections: a bidirectional Mendelian randomization study. Chinese Journal of Respiratory and Critical Care Medicine, 2024, 23(12): 864-875. doi: 10.7507/1671-6205.202406074 Copy

1.	姜旭华, 周静雨, 杨晓菲. 六项呼吸道病原体IgM抗体检测在呼吸道感染中的价值研究. 临床研究, 2024, 32(4): 146-149.
2.	Jin X, Ren J, Li R, et al. Global burden of upper respiratory infections in 204 countries and territories, from 1990 to 2019. EClinicalMedicine, 2021, 37: 100986.
3.	GBD 2016 Lower Respiratory Infections Collaborators. Estimates of the global, regional, and national morbidity, mortality, and aetiologies of lower respiratory infections in 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Infect Dis, 2018, 18(11): 1191-1210.
4.	van Meel ER, Mensink-Bout SM, den Dekker HT, et al. Early-life respiratory tract infections and the risk of school-age lower lung function and asthma: a meta-analysis of 150 000 European children. Eur Respir J, 2022, 60(4): 2102395.
5.	Zhao JH, Stacey D, Eriksson N, et al. Author correction: genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets. Nat Immunol, 2023, 24(11): 1960.
6.	Alosaimi B, Hamed ME, Naeem A, et al. MERS-CoV infection is associated with downregulation of genes encoding Th1 and Th2 cytokines/chemokines and elevated inflammatory innate immune response in the lower respiratory tract. Cytokine, 2020, 126: 154895.
7.	Branchett WJ, Lloyd CM. Regulatory cytokine function in the respiratory tract. Mucosal Immunol, 2019, 12(3): 589-600.
8.	朱鹏飞, 赖晓蓉, 熊沿, 等. 蟛蜞菊内酯通过抑制AMPK/NLRP3/Caspase-1信号通路减轻脂多糖诱导的肺泡上皮细胞焦亡. 中国呼吸与危重监护杂志, 2024, 23(7): 488-494.
9.	Liu C, Chu D, Kalantar-Zadeh K, et al. Cytokines: from clinical significance to quantification. Adv Sci (Weinh), 2021, 8(15): e2004433.
10.	Li Y, Fu X, Ma J, et al. Altered respiratory virome and serum cytokine profile associated with recurrent respiratory tract infections in children. Nat Commun, 2019, 10(1): 2288.
11.	Bohmwald K, Gálvez NMS, Canedo-Marroquín G, et al. Contribution of cytokines to tissue damage during human respiratory syncytial virus infection. Front Immunol, 2019, 10: 452.
12.	Cohen L, Fiore-Gartland A, Randolph AG, et al. A modular cytokine analysis method reveals novel associations with clinical phenotypes and identifies sets of co-signaling cytokines across influenza natural infection cohorts and healthy controls. Front Immunol, 2019, 10: 1338.
13.	Del Valle DM, Kim-Schulze S, Huang HH, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med, 2020, 26(10): 1636-1643.
14.	Baranova A, Luo J, Fu L, et al. Evaluating the effects of circulating inflammatory proteins as drivers and therapeutic targets for severe COVID-19. Front Immunol, 2024, 15: 1352583.
15.	Sanderson E, Glymour MM, Holmes MV, et al. Mendelian randomization. Nat Rev Methods Primers, 2022, 2: 6.
16.	Huang H, Fu Z, Yang M, et al. Levels of 91 circulating inflammatory proteins and risk of lumbar spine and pelvic fractures and peripheral ligament injuries: a two-sample mendelian randomization study. J Orthop Surg Res, 2024, 19(1): 161.
17.	Sanderson E, Spiller W, Bowden J. Testing and correcting for weak and pleiotropic instruments in two-sample multivariable Mendelian randomization. Stat Med, 2021, 40(25): 5434-5452.
18.	Papadimitriou N, Dimou N, Tsilidis KK, et al. Physical activity and risks of breast and colorectal cancer: a Mendelian randomisation analysis. Nat Commun, 2020, 11(1): 597.
19.	Jiang Y, Liu Q, Wang C, et al. The interplay between cytokines and stroke: a bi-directional Mendelian randomization study. Sci Rep, 2024, 14(1): 17657.
20.	Fang P, Liu X, Qiu Y, et al. Exploring causal correlations between inflammatory cytokines and ankylosing spondylitis: a bidirectional mendelian-randomization study. Front Immunol, 2023, 14: 1285106.
21.	Liu W, Wang X, Feng R, et al. Gut microbiota and risk of lower respiratory tract infections: a bidirectional two-sample Mendelian randomization study. Front Microbiol, 2023, 14: 1276046.
22.	Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol, 2015, 44(2): 512-525.
23.	Yao Z, Guo F, Tan Y, et al. Causal relationship between inflammatory cytokines and autoimmune thyroid disease: a bidirectional two-sample Mendelian randomization analysis. Front Immunol, 2024, 15: 1334772.
24.	Didelez V, Sheehan N. Mendelian randomization as an instrumental variable approach to causal inference. Stat Methods Med Res, 2007, 16(4): 309-330.
25.	Heemskerk S, van Heuvel L, Asey T, et al. Disease burden of RSV infections and bronchiolitis in young children (< 5 years) in primary care and emergency departments: a systematic literature review. Influenza Other Respir Viruses, 2024, 18(8): e13344.
26.	Cunningham MJ. The old and new of acute laryngotracheal infections. Clin Pediatr (Phila). 1992, 31(1): 56-64.
27.	Aghasafari P, George U, Pidaparti R. A review of inflammatory mechanism in airway diseases. Inflamm Res, 2019, 68(1): 59-74.
28.	Wang WY, Lim JH, Li JD. Synergistic and feedback signaling mechanisms in the regulation of inflammation in respiratory infections. Cell Mol Immunol, 2012, 9(2): 131-135.
29.	Raffetto JD, Khalil RA. Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease. Biochem Pharmacol, 2008, 75(2): 346-359.
30.	Syed F, Li W, Relich RF, et al. Excessive matrix metalloproteinase-1 and hyperactivation of endothelial cells occurred in COVID-19 patients and were associated with the severity of COVID-19. J Infect Dis, 2021, 224(1): 60-69.
31.	Xu X, Golden JA, Dolganov G, et al. Transcript signatures of lymphocytic bronchitis in lung allograft biopsy specimens. J Heart Lung Transplant, 2005, 24(8): 1055-1066.
32.	Bihlet AR, Karsdal MA, Sand JM, et al. Biomarkers of extracellular matrix turnover are associated with emphysema and eosinophilic-bronchitis in COPD. Respir Res, 2017, 18(1): 22.
33.	Miller MC, Mayo KH. Chemokines from a structural perspective. Int J Mol Sci, 2017, 18(10): 2088.
34.	Bhusal RP, Foster SR, Stone MJ. Structural basis of chemokine and receptor interactions: key regulators of leukocyte recruitment in inflammatory responses. Protein Sci, 2020, 29(2): 420-432.
35.	Oppenheim JJ , Zachariae CO, Mukaida N, et al. Properties of the novel proinflammatory supergene "intercrine" cytokine family. Annu Rev Immunol, 1991, 9: 617-648.
36.	Kim HH, Lee MH, Lee JS. Eosinophil cationic protein and chemokines in nasopharyngeal secretions of infants with respiratory syncytial virus (RSV) bronchiolitis and non-RSV bronchiolitis. J Korean Med Sci, 2007, 22(1): 37-42.
37.	Bachelerie F, Ben-Baruch A, Burkhardt A M, et al. International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. Pharmacological reviews, 2014, 66(1): 1-79.
38.	Harrison AM, Bonville CA, Rosenberg HF, et al. Respiratory syncytical virus-induced chemokine expression in the lower airways: eosinophil recruitment and degranulation. Am J Respir Crit Care Med. 1999, 159(6): 1918-1924.
39.	Domachowske JB, Dyer KD, Bonville CA, et al. Recombinant human eosinophil-derived neurotoxin/RNase 2 functions as an effective antiviral agent against respiratory syncytial virus. J Infect Dis, 1998, 177(6): 1458-1464.
40.	Domachowske JB, Bonville CA, Gao JL, et al. The chemokine macrophage-inflammatory protein-1 alpha and its receptor CCR1 control pulmonary inflammation and antiviral host defense in paramyxovirus infection. J Immunol, 2000, 165(5): 2677-2682.
41.	Li J, Xue L, Wang J, et al. Activation of the chemokine receptor CCR1 and preferential recruitment of Gαi suppress RSV replication: implications for developing novel respiratory syncytial virus treatment strategies. J Virol, 2022, 96(22): e0130922.
42.	王宏宇, 黄海云, 刘晓玲. CCL8相关通路与过敏性疾病. 生命的化学, 2021, 41(10): 2119-2124.
43.	Mindt BC, Fritz JH. Next stop: Perivasculature! ILC2s hitch a ride on the CCL8 express. Sci Immunol, 2019, 4(36): eaax4583.
44.	Puttur F, Denney L, Gregory LG, et al. Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans. Sci Immunol, 2019, 4(36): eaav7638.
45.	Kim J, Kim YS, Ko J. CK beta 8/CCL23 induces cell migration via the Gi/Go protein/PLC/PKC delta/NF-kappa B and is involved in inflammatory responses. Life Sci, 2010, 86(9-10): 300-308.
46.	Guo L, Li N, Yang Z, et al. Role of CXCL5 in regulating chemotaxis of innate and adaptive leukocytes in infected lungs upon pulmonary influenza infection. Front Immunol, 2021, 12: 785457.
47.	Ababneh O, Nishizaki D, Kato S, et al. Tumor necrosis factor superfamily signaling: life and death in cancer. Cancer and Metastasis Reviews, 2024: 1-27.
48.	Fan H, Lu B, Cao C, et al. Plasma TNFSF13B and TNFSF14 function as inflammatory indicators of severe adenovirus pneumonia in pediatric patients. Frontiers in Immunology, 2021, 11: 614781.
49.	Retraction statement: COVID-19 mortality and its predictors in the elderly: a systematic review [retraction of: Health Sci Rep, 2022 May 23, 5(3): e657. doi: 10.1002/hsr2.657]. Health Sci Rep, 2023, 6(7): e1455. doi: 10.1002/hsr2.1455.
50.	Dragovich MA, Mor A. The SLAM family receptors: Potential therapeutic targets for inflammatory and autoimmune diseases. Autoimmun Rev, 2018, 17(7): 674-682.
51.	Liang Z, Zheng X, Wang Y, et al. Using system biology and bioinformatics to identify the influences of COVID-19 co-infection with influenza virus on COPD. Funct Integr Genomics, 2023, 23(2): 175.
52.	Kazmi S, Khan MA, Shamma T, et al. Targeting interleukin-10 restores graft microvascular supply and airway epithelium in rejecting allografts. Int J Mol Sci, 2022, 23(3): 1269.
53.	LeVan TD, Romberger DJ, Siahpush M, et al. Relationship of systemic IL-10 levels with proinflammatory cytokine responsiveness and lung function in agriculture workers. Respir Res, 2018, 19(1): 166.
54.	Sun J, Cardani A, Sharma AK, et al. Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus. PLoS Pathog, 2011, 7(8): e1002173.
55.	Ornitz DM, Itoh N. New developments in the biology of fibroblast growth factors. WIREs Mech Dis, 2022, 14(4): e1549.
56.	Soares-Schanoski A, Sauerwald N, Goforth CW, et al. Asymptomatic SARS-CoV-2 infection is associated with higher levels of serum IL-17C, matrix metalloproteinase 10 and fibroblast growth factors than mild symptomatic COVID-19. Front Immunol, 2022, 13: 821730.

1. 姜旭华, 周静雨, 杨晓菲. 六项呼吸道病原体IgM抗体检测在呼吸道感染中的价值研究. 临床研究, 2024, 32(4): 146-149.
2. Jin X, Ren J, Li R, et al. Global burden of upper respiratory infections in 204 countries and territories, from 1990 to 2019. EClinicalMedicine, 2021, 37: 100986.
3. GBD 2016 Lower Respiratory Infections Collaborators. Estimates of the global, regional, and national morbidity, mortality, and aetiologies of lower respiratory infections in 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Infect Dis, 2018, 18(11): 1191-1210.
4. van Meel ER, Mensink-Bout SM, den Dekker HT, et al. Early-life respiratory tract infections and the risk of school-age lower lung function and asthma: a meta-analysis of 150 000 European children. Eur Respir J, 2022, 60(4): 2102395.
5. Zhao JH, Stacey D, Eriksson N, et al. Author correction: genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets. Nat Immunol, 2023, 24(11): 1960.
6. Alosaimi B, Hamed ME, Naeem A, et al. MERS-CoV infection is associated with downregulation of genes encoding Th1 and Th2 cytokines/chemokines and elevated inflammatory innate immune response in the lower respiratory tract. Cytokine, 2020, 126: 154895.
7. Branchett WJ, Lloyd CM. Regulatory cytokine function in the respiratory tract. Mucosal Immunol, 2019, 12(3): 589-600.
8. 朱鹏飞, 赖晓蓉, 熊沿, 等. 蟛蜞菊内酯通过抑制AMPK/NLRP3/Caspase-1信号通路减轻脂多糖诱导的肺泡上皮细胞焦亡. 中国呼吸与危重监护杂志, 2024, 23(7): 488-494.
9. Liu C, Chu D, Kalantar-Zadeh K, et al. Cytokines: from clinical significance to quantification. Adv Sci (Weinh), 2021, 8(15): e2004433.
10. Li Y, Fu X, Ma J, et al. Altered respiratory virome and serum cytokine profile associated with recurrent respiratory tract infections in children. Nat Commun, 2019, 10(1): 2288.
11. Bohmwald K, Gálvez NMS, Canedo-Marroquín G, et al. Contribution of cytokines to tissue damage during human respiratory syncytial virus infection. Front Immunol, 2019, 10: 452.
12. Cohen L, Fiore-Gartland A, Randolph AG, et al. A modular cytokine analysis method reveals novel associations with clinical phenotypes and identifies sets of co-signaling cytokines across influenza natural infection cohorts and healthy controls. Front Immunol, 2019, 10: 1338.
13. Del Valle DM, Kim-Schulze S, Huang HH, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med, 2020, 26(10): 1636-1643.
14. Baranova A, Luo J, Fu L, et al. Evaluating the effects of circulating inflammatory proteins as drivers and therapeutic targets for severe COVID-19. Front Immunol, 2024, 15: 1352583.
15. Sanderson E, Glymour MM, Holmes MV, et al. Mendelian randomization. Nat Rev Methods Primers, 2022, 2: 6.
16. Huang H, Fu Z, Yang M, et al. Levels of 91 circulating inflammatory proteins and risk of lumbar spine and pelvic fractures and peripheral ligament injuries: a two-sample mendelian randomization study. J Orthop Surg Res, 2024, 19(1): 161.
17. Sanderson E, Spiller W, Bowden J. Testing and correcting for weak and pleiotropic instruments in two-sample multivariable Mendelian randomization. Stat Med, 2021, 40(25): 5434-5452.
18. Papadimitriou N, Dimou N, Tsilidis KK, et al. Physical activity and risks of breast and colorectal cancer: a Mendelian randomisation analysis. Nat Commun, 2020, 11(1): 597.
19. Jiang Y, Liu Q, Wang C, et al. The interplay between cytokines and stroke: a bi-directional Mendelian randomization study. Sci Rep, 2024, 14(1): 17657.
20. Fang P, Liu X, Qiu Y, et al. Exploring causal correlations between inflammatory cytokines and ankylosing spondylitis: a bidirectional mendelian-randomization study. Front Immunol, 2023, 14: 1285106.
21. Liu W, Wang X, Feng R, et al. Gut microbiota and risk of lower respiratory tract infections: a bidirectional two-sample Mendelian randomization study. Front Microbiol, 2023, 14: 1276046.
22. Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol, 2015, 44(2): 512-525.
23. Yao Z, Guo F, Tan Y, et al. Causal relationship between inflammatory cytokines and autoimmune thyroid disease: a bidirectional two-sample Mendelian randomization analysis. Front Immunol, 2024, 15: 1334772.
24. Didelez V, Sheehan N. Mendelian randomization as an instrumental variable approach to causal inference. Stat Methods Med Res, 2007, 16(4): 309-330.
25. Heemskerk S, van Heuvel L, Asey T, et al. Disease burden of RSV infections and bronchiolitis in young children (< 5 years) in primary care and emergency departments: a systematic literature review. Influenza Other Respir Viruses, 2024, 18(8): e13344.
26. Cunningham MJ. The old and new of acute laryngotracheal infections. Clin Pediatr (Phila). 1992, 31(1): 56-64.
27. Aghasafari P, George U, Pidaparti R. A review of inflammatory mechanism in airway diseases. Inflamm Res, 2019, 68(1): 59-74.
28. Wang WY, Lim JH, Li JD. Synergistic and feedback signaling mechanisms in the regulation of inflammation in respiratory infections. Cell Mol Immunol, 2012, 9(2): 131-135.
29. Raffetto JD, Khalil RA. Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease. Biochem Pharmacol, 2008, 75(2): 346-359.
30. Syed F, Li W, Relich RF, et al. Excessive matrix metalloproteinase-1 and hyperactivation of endothelial cells occurred in COVID-19 patients and were associated with the severity of COVID-19. J Infect Dis, 2021, 224(1): 60-69.
31. Xu X, Golden JA, Dolganov G, et al. Transcript signatures of lymphocytic bronchitis in lung allograft biopsy specimens. J Heart Lung Transplant, 2005, 24(8): 1055-1066.
32. Bihlet AR, Karsdal MA, Sand JM, et al. Biomarkers of extracellular matrix turnover are associated with emphysema and eosinophilic-bronchitis in COPD. Respir Res, 2017, 18(1): 22.
33. Miller MC, Mayo KH. Chemokines from a structural perspective. Int J Mol Sci, 2017, 18(10): 2088.
34. Bhusal RP, Foster SR, Stone MJ. Structural basis of chemokine and receptor interactions: key regulators of leukocyte recruitment in inflammatory responses. Protein Sci, 2020, 29(2): 420-432.
35. Oppenheim JJ , Zachariae CO, Mukaida N, et al. Properties of the novel proinflammatory supergene "intercrine" cytokine family. Annu Rev Immunol, 1991, 9: 617-648.
36. Kim HH, Lee MH, Lee JS. Eosinophil cationic protein and chemokines in nasopharyngeal secretions of infants with respiratory syncytial virus (RSV) bronchiolitis and non-RSV bronchiolitis. J Korean Med Sci, 2007, 22(1): 37-42.
37. Bachelerie F, Ben-Baruch A, Burkhardt A M, et al. International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. Pharmacological reviews, 2014, 66(1): 1-79.
38. Harrison AM, Bonville CA, Rosenberg HF, et al. Respiratory syncytical virus-induced chemokine expression in the lower airways: eosinophil recruitment and degranulation. Am J Respir Crit Care Med. 1999, 159(6): 1918-1924.
39. Domachowske JB, Dyer KD, Bonville CA, et al. Recombinant human eosinophil-derived neurotoxin/RNase 2 functions as an effective antiviral agent against respiratory syncytial virus. J Infect Dis, 1998, 177(6): 1458-1464.
40. Domachowske JB, Bonville CA, Gao JL, et al. The chemokine macrophage-inflammatory protein-1 alpha and its receptor CCR1 control pulmonary inflammation and antiviral host defense in paramyxovirus infection. J Immunol, 2000, 165(5): 2677-2682.
41. Li J, Xue L, Wang J, et al. Activation of the chemokine receptor CCR1 and preferential recruitment of Gαi suppress RSV replication: implications for developing novel respiratory syncytial virus treatment strategies. J Virol, 2022, 96(22): e0130922.
42. 王宏宇, 黄海云, 刘晓玲. CCL8相关通路与过敏性疾病. 生命的化学, 2021, 41(10): 2119-2124.
43. Mindt BC, Fritz JH. Next stop: Perivasculature! ILC2s hitch a ride on the CCL8 express. Sci Immunol, 2019, 4(36): eaax4583.
44. Puttur F, Denney L, Gregory LG, et al. Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans. Sci Immunol, 2019, 4(36): eaav7638.
45. Kim J, Kim YS, Ko J. CK beta 8/CCL23 induces cell migration via the Gi/Go protein/PLC/PKC delta/NF-kappa B and is involved in inflammatory responses. Life Sci, 2010, 86(9-10): 300-308.
46. Guo L, Li N, Yang Z, et al. Role of CXCL5 in regulating chemotaxis of innate and adaptive leukocytes in infected lungs upon pulmonary influenza infection. Front Immunol, 2021, 12: 785457.
47. Ababneh O, Nishizaki D, Kato S, et al. Tumor necrosis factor superfamily signaling: life and death in cancer. Cancer and Metastasis Reviews, 2024: 1-27.
48. Fan H, Lu B, Cao C, et al. Plasma TNFSF13B and TNFSF14 function as inflammatory indicators of severe adenovirus pneumonia in pediatric patients. Frontiers in Immunology, 2021, 11: 614781.
49. Retraction statement: COVID-19 mortality and its predictors in the elderly: a systematic review [retraction of: Health Sci Rep, 2022 May 23, 5(3): e657. doi: 10.1002/hsr2.657]. Health Sci Rep, 2023, 6(7): e1455. doi: 10.1002/hsr2.1455.
50. Dragovich MA, Mor A. The SLAM family receptors: Potential therapeutic targets for inflammatory and autoimmune diseases. Autoimmun Rev, 2018, 17(7): 674-682.
51. Liang Z, Zheng X, Wang Y, et al. Using system biology and bioinformatics to identify the influences of COVID-19 co-infection with influenza virus on COPD. Funct Integr Genomics, 2023, 23(2): 175.
52. Kazmi S, Khan MA, Shamma T, et al. Targeting interleukin-10 restores graft microvascular supply and airway epithelium in rejecting allografts. Int J Mol Sci, 2022, 23(3): 1269.
53. LeVan TD, Romberger DJ, Siahpush M, et al. Relationship of systemic IL-10 levels with proinflammatory cytokine responsiveness and lung function in agriculture workers. Respir Res, 2018, 19(1): 166.
54. Sun J, Cardani A, Sharma AK, et al. Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus. PLoS Pathog, 2011, 7(8): e1002173.
55. Ornitz DM, Itoh N. New developments in the biology of fibroblast growth factors. WIREs Mech Dis, 2022, 14(4): e1549.
56. Soares-Schanoski A, Sauerwald N, Goforth CW, et al. Asymptomatic SARS-CoV-2 infection is associated with higher levels of serum IL-17C, matrix metalloproteinase 10 and fibroblast growth factors than mild symptomatic COVID-19. Front Immunol, 2022, 13: 821730.

Chinese Journal of Respiratory and Critical Care Medicine

Causality between 91 circulating inflammatory proteins and respiratory infections: a bidirectional Mendelian randomization study

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