Irsogladine maleate influences the response of gap junctional intercellular communication and IL-8 of human gingival epithelial cells following periodontopathogenic bacterial challenge

Uchida, Yuushi; Shiba, Hideki; Komatsuzawa, Hitoshi; Hirono, Chikara; Ashikaga, Arata; Fujita, Tsuyoshi; Kawaguchi, Hiroyuki; Sugai, Motoyuki; Shiba, Yoshiki; Kurihara, Hidemi

doi:10.1016/j.bbrc.2005.05.147

Cited by 31 publications

(49 citation statements)

References 26 publications

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“…This is associated with downregulated levels of phosphorylated and non-phosphorylated Cx43 protein and concomitant lowered cAMP amounts. In the same study, it was also demonstrated that the anti-ulcer agent irsogladine maleate is able to counteract the deleterious actions of OMP29 on Cx43-based gap junctions [118].…”

Section: Aggregatibacter (Actinobacillus) Actinomycetemcomitansmentioning

confidence: 85%

“…The anticonvulsant levetiracetam [33] and the glucocorticoid dexamethasone [34], for example, were both reported to alleviate LPS-induced reduction of GJIC and Cx43 expression levels in co-cultures of primary rat astroglial cells and primary rat microglial cells. Similarly, abrogation of GJIC and Cx43 production in human gingival epithelial cells exposed to A. actinomycetemcomitans-derived OMP29 could be counteracted by the anti-ulcer agent irsogladine maleate [118]. On the other hand, the effects of bacteria on connexin signaling might be exploited in cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of connexin signaling by bacterial pathogens and their toxins

Ceelen

Haesebrouck

Vanhaecke

et al. 2011

Cell. Mol. Life Sci.

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Inherent to their pivotal tasks in the maintenance of cellular homeostasis, gap junctions, connexin hemichannels, and pannexin hemichannels are frequently involved in the dysregulation of this critical balance. The present paper specifically focuses on their roles in bacterial infection and disease. In particular, the reported biological outcome of clinically important bacteria including Escherichia coli, Shigella flexneri, Yersinia enterocolitica, Helicobacter pylori, Bordetella pertussis, Aggregatibacter actinomycetemcomitans, Pseudomonas aeruginosa, Citrobacter rodentium, Clostridium species, Streptococcus pneumoniae, and Staphylococcus aureus and their toxic products on connexin- and pannexin-related signaling in host cells is reviewed. Particular attention is paid to the underlying molecular mechanisms of these effects as well as to the actual biological relevance of these findings.

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Section: Aggregatibacter (Actinobacillus) Actinomycetemcomitansmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Modulation of connexin signaling by bacterial pathogens and their toxins

Ceelen

Haesebrouck

Vanhaecke

et al. 2011

Cell. Mol. Life Sci.

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“…GT1 was cultured with Dulbecco's modified Eagle's medium (Sigma Chemical Co., St. Louis, MO, USA) containing 10% fetal calf serum, 100 U/mL penicillin, and 100 mg/mL streptomycin. We also prepared a primary culture of human gingival keratinocytes and fibroblasts (Kamata et al, 2004;Uchida et al, 2005). Informed consent for the acquisition was obtained under a protocol approved by the Ethical Committee of Hiroshima University.…”

Section: Cell Linesmentioning

confidence: 99%

Regulation of CXCL9/10/11 in Oral Keratinocytes and Fibroblasts

et al. 2008

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Th1 and Th2 cytokines such as interferon-gamma (IFN-gamma ) , tumor necrosis factor- alpha (TNF-alpha ), and IL-4 are expressed in T-cell-mediated inflammation in the oral cavity. We tested the hypothesis that those cytokines may act on CXCR3-agonistic chemokines, T-cell recruiting factors, and on neighboring cells, including oral keratinocytes and fibroblasts. Human immortalized oral keratinocytes (RT7) and fibroblasts (GT1) after 24-hour stimulation with IFN-gamma showed increased mRNA levels of CXCL9 (600- and 700-fold), CXCL10 (10,000- and 150-fold), and CXCL11 (5000- and 300-fold), respectively. In contrast, TNF-alpha caused an increase in CXCL9 (300-fold), CXCL10 (2000-fold), and CXCL11 (2000-fold) mRNA levels in GT1, but not RT7 cells, at 24 hrs. IL-4 reinforced the promotion of CXCL9, CXCL10, and CXCL11 expression by IFN-gamma in RT7 cells, whereas IL-4 inhibited the increased levels by IFN-gamma and TNF-alpha in GT1 cells. Thus, IFN-gamma , TNF-alpha , and IL-4 appear cooperatively to regulate CXCR3-agonistic chemokines in oral keratinocytes and fibroblasts in T-cell-mediated oral inflammation sites.

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“…We have investigated the effect of IM on the interaction between human gingival epithelial cells (HGEC) and periodontopathogenic bacteria to clarify whether IM could help to prevent periodontal disease. Exposure of HGEC to outer membrane protein (OMP) 29 from Aggregatibacter ( Actinobacillus ) actinomycetemcomitans or whole live A. actinomycetemcomitans increases IL‐8 secretion and inhibits gap junctional intercellular communication (4). IM obviates the increase in IL‐8 levels and recovers the reduction of gap junctional intercellular communication in HGEC stimulated by OMP29 or A. actinomycetemcomitans (4).…”

mentioning

confidence: 99%