JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2016, Vol. 54 ›› Issue (3): 9-13.doi: 10.6040/j.issn.1671-7554.0.2015.750

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Effect of Helicobacter pylori infection on NLRP3 inflammasome activation

LIU Zhengmei, JIANG qiong, ZHOU Jianjiang, GUAN Zhizhong, ZHAO Yan, XIONG Lin, XIE Yuan   

  1. Key Laboratory of Molecular Biology, Guizhou Medical University, Guiyang 550004, Guizhou, China
  • Received:2015-08-10 Online:2016-03-10 Published:2016-03-10

Abstract: Objective To study the impact of Helicobacter pylori(H.pylori) infection on NLRP3 inflammasome associated proteins expression and activation in gastric epithelial cells and gastric cancer cells, and further discuss the role of NLRP3 inflammasome when gastric cells were infected by H.pylori. Methods The gastric epithelial cell line GES-1 and gastric cancer cell line MKN-45 were infected by H.pylori NCTC11639 at a multiplicity of infection(MOI)of 100 or 200. At 6 h or 12 h after infection, the cells were harvested and the total proteins were extracted. Then the expressions of NLRP3 and Caspase-1 were analyzed by Western blotting and the level of IL-1β secretion was detected by ELISA. Results The expressions of NLRP3 and Caspase-1 and the secretion of IL-1β were increased with the increase of NCTC11639 MOI in GES-1 cells(P<0.05). Although the expression of NLRP3 was increased, the expression of Caspase-1 and the secretion of IL-1β were decreased with the increase of NCTC11639 MOI in MKN-45 cells(P<0.05). In addition, the expressions of NLRP3 and Caspase-1 and the secretion of IL-1β were not significantly different in GES-1 or MKN-45 infected by H.pylori for 6 h and 12 h with the same MOI(P>0.05). Conclusion H.pylori infection promotes the expressions and activations of NLRP3, Caspase-1 and IL-1β in gastric epithelial cells. However, H.pylori infection facilitates the expression of NLRP3 but inhibits the expressions and activations of Caspase-1 and IL-1β in gastric cancer cells.

Key words: Helicobacter pylori, Caspase-1, NLRP3, IL-1β

CLC Number: 

  • R735.2
[1] Forman D, Newell DG, Fullerton F, et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation[J]. BMJ, 1991, 302(6788):1302-1305.
[2] Kawai T, Akira S. Toll-like receptor and RIG-1-like receptor signaling[J]. Annals of the New York Academy of Sciences, 2008, 1143(1):1-20.
[3] Schroder K, Tschopp J. The inflammasomes[J]. Cell, 2010, 140(6):821-832.
[4] Plummer M, van Doorn LJ, Franceschi S, et al. Helicobacter pylori cytotoxin-associated genotype and gastric precancerous lesions[J]. J Natl Cancer Inst, 2007, 99(17):1328-1334.
[5] Jacobs SR, Damania B. NLRs, inflammasomes, and viral infection[J]. J Leukoc Biol, 2012, 92(3):469-477.
[6] Costa A, Gupta R, Signorino G, et al. Activation of the NLRP3 inflammasome by group B streptococci[J]. J Immunol, 2012, 188(4):1953-1960.
[7] Serelli-Lee V, Ling KL, Ho C, et al. Persistent Helicobacter pylori specific Th17 responses in patients with past H.pylori infection are associated with elevated gastric mucosal IL-1beta[J]. PLoS One, 2012, 7(6): e39199. doi:10.1371/journal.pone.0039199.
[8] Romero-Adrian TB, Leal-Montiel J, Monsalve-Castillo F, et al. Helicobacter pylori: bacterial factors and the role of cytokines in the immune response[J]. Curr Microbiol, 2010, 60(2):143-155.
[9] Hong SN, Jo S, Jang JH, et al. Clinical characteristics and the expression profiles of inflammatory cytokines /cytokine regulatory factors in asymptomatic patients with nodular gastritis[J]. Dig Dis Sci, 2012, 57(6):1486-1495.
[10] Brown DI, Griendling KK. Nox proteins in signal transduction[J]. Free Radic Biol Med, 2009, 47(9):1239-1253.
[11] Hitzler I, Sayi A, Kohler E, et al. Caspase-1 has both proinflammatory and regulatory properties in Helicobacter infections, which are differentially mediated by its substrates IL-1beta and IL-18[J]. J Immunol, 2012, 188(8):3594-3602.
[12] 邝玉,杨远,李婉宜,等. 幽门螺杆菌体外培养影响因素探讨[J].中国病原生物学杂志,2013,8(7):595-597. KUANG Yu, YANG Yuan, LI Wanyi, et al. Study of factors affecting the in vitro culture of Helicobacter pylori[J]. Journal of Pathogen Biology, 2013, 8(7):595-597.
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