Journal of Microbiology

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Cot kinase plays a critical role in Helicobacter pylori-induced IL-8 expression: Sungil Jang , Jinmoon Kim , Jeong-Heon Cha; J. Microbiol. 2017;55(4):311-317. Published online March 31, 2017; DOI: https://doi.org/10.1007/s12275-017-7052-9

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Helicobacter pylori is a major pathogen causing various gastric diseases including gastric cancer. Infection of H. pylori induces pro-inflammatory cytokine IL-8 expression in gastric epithelial cells in the initial inflammatory process. It has been known that H. pylori can modulate Ras-Raf-Mek-Erk signal pathway for IL-8 induction. Recently, it has been shown that another signal molecule, cancer Osaka thyroid oncogene/tumor progression locus 2 (Cot/Tpl2) kinase, activates Mek and Erk and plays a role in the Erk pathway, similar to MAP3K signal molecule Raf kinase. Therefore, the objective of this study was to determine whether Cot kinase might be involved in IL-8 induction caused by H. pylori infection. AGS gastric epithelial cells were infected by H. pylori strain G27 or its isogenic mutants lacking cagA or type IV secretion system followed by treatment with Cot kinase inhibitor (KI) or siRNA specific for Cot kinase. Activation of Erk was assessed by Western blot analysis and expression of IL-8 was measured by ELISA. Treatment with Cot KI reduced both transient and sustained Erk activation. It also reduced early and late IL-8 secretion in the gastric epithelial cell line. Furthermore, siRNA knockdown of Cot inhibited early and late IL-8 secretion induced by H. pylori infection. Taken together, these results suggest that Cot kinase might play a critical role in H. pylori type IV secretion apparatus-dependent early IL-8 secretion and CagA-dependent late IL-8 secretion as an alternative signaling molecule in the Erk pathway.

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Use of Selected Lactic Acid Bacteria in the Eradication of Helicobacter pylori Infection: Jin-Eung Kim , Min-Soo Kim , Yeo-Sang Yoon , Myung-Jun Chung , Do-Young Yum; J. Microbiol. 2014;52(11):955-962. Published online October 3, 2014; DOI: https://doi.org/10.1007/s12275-014-4355-y

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Abstract

Helicobacter pylori is among the major pathogenic bacteria that cause chronic gastritis and peptic ulcer disease and is related to the development of gastric cancer. Several chemicals, including antibiotics, have been used to eradicate H. pylori; however, they do not always curb the infection. Ten representative type strains of lactic acid bacteria (LAB) were screened for antagonism toward H. pylori via inhibition of urease activity. Strains inhibiting the binding of H. pylori to human gastric cell line cells and suppressing H. pylori-induced interleukin-8 (IL-8) production were also screened. Of these, Pediococcus pentosaseus (SL4), which inhibited the adhesion of H. pylori to MKN-45 gastric cancer cells, Bifidobacterium longum (BG7), with urease inhibiting activity, and Lactococcus lactis (SL3), and Enterococcus faecalis (SL5), which suppressed H. pylori-induced IL-8 production within MKN-45 and AGS cells, were selected. In mouse model, these LAB stains in combination significantly suppressed IL-8 levels in serum. Gastric pH also recovered to normal values after the administration of these LAB. These stains effectively suppressed H. pylori viability, although not to the extent of antibiotic treatment. When used as probiotics, LAB may help decrease the occurrence of gastritis and reduce the risk of H. pylori infection without, inducing side effects.

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Induction of IL-8 in Periodontal Ligament Cells by H2O2: Yang-Sin Lee , Eun Jung Bak , Minyoung Kim , Wonse Park , Jeong Taeg Seo , Yun-Jung Yoo; J. Microbiol. 2008;46(5):579-584. Published online October 31, 2008; DOI: https://doi.org/10.1007/s12275-008-0182-3

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Abstract: Periodontitis is an inflammatory disease caused by bacteria. In periodontitis, reactive oxygen species (ROS) are released from inflammatory cells in response to bacteria. Interleukin (IL)-8 is one of pro-inflammatory cytokines. To investigate the role of ROS in pathogenesis of periodontitis, we estimated the effect of H2O2, one of ROS, on the expression of IL-8 in human periodontal ligament (PDL) cells. PDL cells were treated with H2O2. IL-8 expression was determined by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38) and c-jun NH2-terminal kinase (JNK) was estimated by Western blotting. Treatment with H2O2 at concentration of up to 250 μM increased IL-8 mRNA expression and production in a concentration-dependent manner. However, treatment with 500 μM H2O2 did not increase IL-8 production. Catalase, an inhibitor of H2O2, down-regulated the production of IL-8 induced by H2O2. H2O2 increased the phosphorylation of ERK, p38, and JNK. Pretreatment with PD98059 (ERK inhibitor), SB203580 (p38 inhibitor), or SP600125 (JNK inhibitor) decreased the IL-8 production induced by H2O2. These results indicate that H2O2 acts as an inducer of IL-8 secretion via activation of ERK, p38, and JNK in PDL cells. H2O2 deposited in periodontal tissue during inflammation against bacteria may accelerate tissue destruction via induction of IL-8 in PDL cells.

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