Protective effect of interleukin-26 on the lipopolysaccharides-induced late lung injury_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

RAO Yafei , ZHANG Hui ,  BAO Aihua ^饒 ,  WANG Jing

The Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P. R. China;

Corresponding?author：

BAO Aihua, Email: aihuabao312@126.com; WANG Jing, Email: wangjing@zzu.edu.cn

Keywords：

Interleukin 26; Lipopolysaccharides; Lung injury; Inflammation

DOI：

10.7507/1671-6205.201901040

Video：

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Objective To investigate the effects of interleukin (IL)-26 on the late phase of lipopolysaccharides (LPS)-induced lung inflammation in mouse model.Methods Thirty-two mice were equally and randomly divided into four groups: blank control group, IL-26 control group, LPS model group, and IL-26 intervention group. The blank control group was given intranasal administration of phosphate buffered solution (PBS, 40 μl) and PBS (40 μl) 10 minutes apart. The IL-26 control group was given recombinant human interleukin-26 (rhIL-26; 50 μg/kg, dissolved in 40 μg PBS) and PBS successively. The LPS model group was given intranasal administration of PBS (40 μl) and LPS (10 mg/kg, dissolved in 40 μl PBS) at 10 minutes interval. The IL-26 intervention group was given intranasal administration of rhIL-26 and LPS at 10 minutes interval. Seventy-two hours later after treatment, bronchoalveolar lavage fluid (BALF) cell count, cytokine assay and pathological staining of lung tissue were performed in each group. The gene expression of inflammatory pathway in lung tissue was detected by RT-PCR. One-way ANOVA was used for comparison between groups. Results Compared with the blank control group, the expression of tumor necrosis factor-α and activating transcription factor 3 in IL-26 control group increased significantly (all P < 0.05). The number of peripheral blood mononuclear cells, total BALF cells, lymphocytes and neutrophils, and the content of macrophage inflammatory protein-1a in BALF were significantly increased in IL-26 intervention group comparing with LPS model group (all P < 0.05). IL-26 intervention group had more inflammatory subsidence in interstitial, perivascular, peribronchial and mean values than LPS model group (all P < 0.05). The expressions of Toll-like receptor 4, Toll-like receptor 2 and interferon γ induced protein 10 in IL-26 intervention group were significantly higher than those in LPS model group (all P < 0.05).Conclusion IL-26 can significantly alleviate the late inflammatory reaction of lung tissue in LPS-induced mouse inflammation model.

Citation： RAO Yafei, ZHANG Hui, BAO Aihua, WANG Jing. Protective effect of interleukin-26 on the lipopolysaccharides-induced late lung injury. Chinese Journal of Respiratory and Critical Care Medicine, 2019, 18(3): 259-264. doi: 10.7507/1671-6205.201901040 Copy

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2.	Che KF, Tengvall S, Levanen B, et al. Interleukin-26 in antibacterial host defense of human lungs. Effects on neutrophil mobilization. Am J Respir Crit Care Med, 2014, 190(9): 1022-1031.
3.	Bao A, Che KF, Bozinovski S, et al. Recombinant human IL-26 facilitates the innate immune response to endotoxin in the bronchoalveolar space of mice in vivo. PLoS One, 2017, 12(12): e0188909.
4.	Cui SN, Chen L, Yang YY, et al. Activation of death-associated protein kinase 1 promotes neutrophil apoptosis to accelerate inflammatory resolution in acute respiratory distress syndrome. Lab Invest, 2019. [Epub ahead of print].
5.	Wang CN, Lin YC, Chang BC, et al. Targeting the phosphorylation site of myristoylated alanine-rich C kinase substrate alleviates symptoms in a murine model of steroid-resistant asthma. Br J Pharmacol, 2019, 176(8): 1122-1134.
6.	Fang H, Hua C, Weiss S, et al. Modulation of innate immunity by G-CSF and inflammatory response by LBPK95A improves the outcome of sepsis in a rat model. J Immunol Res, 2018: 6085095.
7.	Denning NL, Yang WL, Hansen L, et al. C23, an oligopeptide derived from cold-inducible RNA-binding protein, suppresses inflammation and reduces lung injury in neonatal sepsis. J Pediatr Surg, 2019, pii: S0022-3468(18)30885-6.
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11.	Su YC, Jalalvand F, Thegerstrom J, et al. The interplay between immune response and bacterial infection in COPD: focus upon non-typeable Haemophilus influenzae. Front Immunol, 2018, 9: 2530.
12.	Tillotson GS, Zinner SH. Burden of antimicrobial resistance in an era of decreasing susceptibility. Expert Rev Anti Infect Ther, 2017, 15(7): 663-676.
13.	Jatzlauk G, Bartel S, Heine H, et al. Influences of environmental bacteria and their metabolites on allergies, asthma, and host microbiota. Allergy, 2017, 72(12): 1859-1867.
14.	Tengvall S, Che KF, Lindén A, et al. Interleukin-26: an emerging player in host defense and inflammation. J Innate Immun, 2016, 8(1): 15-22.
15.	Wu Y, Wang L, Meng L, et al. MIP-1α and NF-κB as indicators of acute kidney injury secondary to acute lung injury in mechanically ventilated patients. Eur Rev Med Pharmacol Sci, 2016, 20(18): 3830-3834.
16.	Katsura H, Kobayashi Y, Tata PR, et al. IL-1 and TNFα contribute to the inflammatory niche to enhance alveolar regeneration. Stem Cell Reports, 2019, 12(4): 657-666.
17.	Fei D, Meng X, Yu W, et al. Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin beta1. Virulence, 2018, 9(1): 1588-1600.
18.	Akram A, Han B, Masoom H, et al. Activating transcription factor 3 confers protection against ventilator-induced lung injury. Am J Respir Crit Care Med, 2010, 182(4): 489-500.
19.	Matsuki A, Takatori H, Makita S, et al. T-bet inhibits innate lymphoid cell-mediated eosinophilic airway inflammation by suppressing IL-9 production. J Allergy Clin Immunol, 2017, 139(4): 1355-1367. e6.
20.	Miyamoto C, Kojo S, Yamashita M, et al. Author Correction: Runx/Cbfβ complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation. Nat Commun, 2019, 10(1): 1075.
21.	Monin L, Mehta S, Elsegeiny W, et al. Aspergillus fumigatus preexposure worsens pathology and improves control of Mycobacterium abscessus pulmonary infection in mice. Infect Immun, 2018, 86(3): pii: e00859-17.

1. Wilson NJ, Boniface K, Chan JR, et al. Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol, 2007, 8(9): 950-957.
2. Che KF, Tengvall S, Levanen B, et al. Interleukin-26 in antibacterial host defense of human lungs. Effects on neutrophil mobilization. Am J Respir Crit Care Med, 2014, 190(9): 1022-1031.
3. Bao A, Che KF, Bozinovski S, et al. Recombinant human IL-26 facilitates the innate immune response to endotoxin in the bronchoalveolar space of mice in vivo. PLoS One, 2017, 12(12): e0188909.
4. Cui SN, Chen L, Yang YY, et al. Activation of death-associated protein kinase 1 promotes neutrophil apoptosis to accelerate inflammatory resolution in acute respiratory distress syndrome. Lab Invest, 2019. [Epub ahead of print].
5. Wang CN, Lin YC, Chang BC, et al. Targeting the phosphorylation site of myristoylated alanine-rich C kinase substrate alleviates symptoms in a murine model of steroid-resistant asthma. Br J Pharmacol, 2019, 176(8): 1122-1134.
6. Fang H, Hua C, Weiss S, et al. Modulation of innate immunity by G-CSF and inflammatory response by LBPK95A improves the outcome of sepsis in a rat model. J Immunol Res, 2018: 6085095.
7. Denning NL, Yang WL, Hansen L, et al. C23, an oligopeptide derived from cold-inducible RNA-binding protein, suppresses inflammation and reduces lung injury in neonatal sepsis. J Pediatr Surg, 2019, pii: S0022-3468(18)30885-6.
8. Faller S, Hausler F, Goeft A, et al. Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury. Sci Rep, 2018, 8(1): 14676.
9. Santiago V, Rezvani K, Sekine T, et al. Human NK cells develop an exhaustion phenotype during polar degranulation at the Aspergillus fumigatus hyphal synapse. Front Immunol, 2018, 9: 2344.
10. Matute-Bello G, Downey G, Moo BB, et al. An official American Thoracic Society workshop report: features and measurements of experimental acute lung injury in animals. Am J Respir Crit Care Med, 2011, 44(5): 725-738.
11. Su YC, Jalalvand F, Thegerstrom J, et al. The interplay between immune response and bacterial infection in COPD: focus upon non-typeable Haemophilus influenzae. Front Immunol, 2018, 9: 2530.
12. Tillotson GS, Zinner SH. Burden of antimicrobial resistance in an era of decreasing susceptibility. Expert Rev Anti Infect Ther, 2017, 15(7): 663-676.
13. Jatzlauk G, Bartel S, Heine H, et al. Influences of environmental bacteria and their metabolites on allergies, asthma, and host microbiota. Allergy, 2017, 72(12): 1859-1867.
14. Tengvall S, Che KF, Lindén A, et al. Interleukin-26: an emerging player in host defense and inflammation. J Innate Immun, 2016, 8(1): 15-22.
15. Wu Y, Wang L, Meng L, et al. MIP-1α and NF-κB as indicators of acute kidney injury secondary to acute lung injury in mechanically ventilated patients. Eur Rev Med Pharmacol Sci, 2016, 20(18): 3830-3834.
16. Katsura H, Kobayashi Y, Tata PR, et al. IL-1 and TNFα contribute to the inflammatory niche to enhance alveolar regeneration. Stem Cell Reports, 2019, 12(4): 657-666.
17. Fei D, Meng X, Yu W, et al. Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin beta1. Virulence, 2018, 9(1): 1588-1600.
18. Akram A, Han B, Masoom H, et al. Activating transcription factor 3 confers protection against ventilator-induced lung injury. Am J Respir Crit Care Med, 2010, 182(4): 489-500.
19. Matsuki A, Takatori H, Makita S, et al. T-bet inhibits innate lymphoid cell-mediated eosinophilic airway inflammation by suppressing IL-9 production. J Allergy Clin Immunol, 2017, 139(4): 1355-1367. e6.
20. Miyamoto C, Kojo S, Yamashita M, et al. Author Correction: Runx/Cbfβ complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation. Nat Commun, 2019, 10(1): 1075.
21. Monin L, Mehta S, Elsegeiny W, et al. Aspergillus fumigatus preexposure worsens pathology and improves control of Mycobacterium abscessus pulmonary infection in mice. Infect Immun, 2018, 86(3): pii: e00859-17.

Chinese Journal of Respiratory and Critical Care Medicine

Protective effect of interleukin-26 on the lipopolysaccharides-induced late lung injury

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