Hideo Shigeishi

Queen Mary, University of London, Londinium, England, United Kingdom

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Publications (46)128.81 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Malignant salivary gland tumors are rare and exhibit a broad spectrum of phenotypic heterogeneity. The objective of this study was to investigate prognostic factors in patients with salivary gland carcinomas and review the results in light of other reports. We retrospectively reviewed 40 patients with primary salivary gland carcinomas who were diagnosed and treated at our institution between 1991 and 2014. Of the 40 tumors, 19 (47.5%) were mucoepidermoid carcinomas, 11 (27.5%) were adenoid cystic carcinomas, 7 (17.5%) were acinic cell carcinomas, 2 (5.0%) were myoepithelial carcinomas and 1 (2.5%) was a squamous cell carcinoma. Clinically positive lymph nodes were present in 4 patients (10.0%). As regards clinical stage, 15 cases (37.5%) were stage I, 13 (32.5%) were stage II, 1 (2.5%) was stage III and 11 (27.5%) were stage IVA. The majority of the patients (97.5%) were treated with surgery, of whom 25 (62.5%) received surgery alone and 14 (35.0%) underwent surgery in combination with chemotherapy or chemotherapy and radiotherapy. The median follow-up time for all the patients was 48 months. The disease-specific survival rate at 5 years was 87.1%. We identified a significant correlation between poor survival rate and histological grade (intermediate/high), tumor size (T3/T4), lymph node metastasis (node-positive) and clinical stage (III/IV) using the Kaplan-Meier method (P<0.05 for each). In addition, the Cox proportional hazards regression analysis confirmed that lymph node metastasis and tumor size were independent prognostic factors for disease-specific survival (hazard ratio = 18.7 and 15.1, respectively; P=0.023 and 0.037, respectively). Furthermore, tumor size was found to be a predictive factor regarding recurrence in the multivariate logistic regression analysis (odds ratio = 8.35; P=0.025). Our results suggest that lymph node metastasis and tumor size are significant prognostic factors for patients with salivary gland carcinomas.
    Molecular and clinical oncology. 01/2015; 3(1):202-206.
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    ABSTRACT: Background: Innate immune response by oral mucosal cells may be the first line of host defense against viral infection. Retinoic acid-inducible gene-I (RIG-I) recognizes viral dsRNA in the cytoplasm, and RIG-I-mediated signaling regulates antiviral type I IFN, and inflammatory chemokine production. Here, we tested the hypothesis that oral mucosal cell participation in host defense against viral infection via RIG-I. Methods: RIG-I expression was detected in immortalized oral keratinocytes (RT7), oral fibroblasts (GT1) using and RT-PCR and immunohistochemistry. RT7 and GT1 were exposed to dsRNA virus mimic Poly I:C-LMW/LyoVec (PLV). Expression of IFN-β and CXCL10 via RIG-I was examined by Real-time RT-PCR and ELISA. Phosphorylation of IRF3 and STAT1 were detected by western blotting. Results: RT7 and GT1 constitutively expressed RIG-I in the cytoplasm. Furthermore, PLV increased IFN-β and CXCL10 productions in both RT7 and GT1 via RIG-I concurrent with phosphorylation of IRF3 and STAT1. PLV-induced CXCL10 production was attenuated by neutralization of IFN-β and blocking of IFN-α/β receptor (IFNAR), indicating primal IFN-β production via the RIG-I-IRF3 axis, which eventually induces CXCL10 production via the IFNAR -STAT1 axis. Conclusion: We propose that RIG-I in oral keratinocytes and fibroblasts may cumulatively develop host-defense mechanisms against viral infection in oral mucosa. © 2014 S. Karger AG, Basel.
    Journal of Oral and Maxillofacial Surgery 10/2014; 34(5):1556-1565. · 1.28 Impact Factor
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    ABSTRACT: Background Cancer stem cells (CSCs) are involved in both tumourigenesis and in tumour recurrence after therapy. In head and neck squamous cell carcinoma (HNSCC), there are two biologically different CSC phenotypes both of which express high levels of CD44 but differ in their expression levels of epithelial-specific antigen (ESA). One phenotype is CD44high/ESAhigh and has epithelial features (Epi-CSCs), while the other is CD44high/ESAlow, has undergone epithelial to mesenchymal transition (EMT-CSCs), has mesenchymal features and is migratory (Biddle et al., 2011). CSCs are resistant to therapeutically induced apoptosis but the molecular mechanisms by which they develop apoptotic resistance remains unclear. However, glycogen synthase kinase 3β (GSK3β) contributes to regulation of both the self-renewal and switching of these two CSC phenotypes (Shigeishi et al., 2013).MethodsCD44high/ESAlow, CD44high/ESAhigh and CD44low cells were FACS sorted from the HNSCC cell line LUC4, and 5-FU-induced apoptosis was analysed by Annexin V staining followed by flow cytometry analysis.ResultsCD44high/ESAlow cells exhibited marked resistance to 5-FU-induced apoptosis and had high expression of dihydropyrimidine dehydrogenase (DPD). The DPD inhibitor, 5-chloro-2, 4-dihydroxypyridine (CDHP) significantly enhanced 5-FU-induced apoptosis of CD44high/ESAlow cells. Inhibition of GSK3β induced CD44high/ESAlow cells to undergo mesenchymal-to-epithelial transition (MET) to CD44high/ESAhigh cells and pre-existing CD44high/ESAhigh cells to differentiate. Apoptosis induced by 5-FU was thus facilitated. Combination of both CDHP and GSK3β inhibitors markedly enhanced 5-FU-induced apoptosis of CD44high/ESAlow cells.Conclusions Our results suggest potentially new approaches for the elimination of the therapy resistant HNSCC CSC population.
    Journal of Oral Pathology and Medicine 08/2014; · 2.06 Impact Factor
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    ABSTRACT: The receptor for hyaluronan (HA)-mediated motility (RHAMM) is a HA-binding protein located in the cytoskeleton and centrosome. RHAMM has multiple functions that manifest with different cellular localizations, for example, modulation of growth factor receptor, regulation of cell signaling pathways, and mitotic spindle assembly. In addition, its increased expression has major roles in tumorigenesis and can induce genomic instability and cancer progression. In head and neck cancers, increased expression of RHAMM is associated with high proliferation of cancer cells and decreased survival. CD44, a cell-adhesion molecule and HA receptor, can modulate intracellular signaling by forming complexes with RHAMM to promote invasion and metastasis of cancer cells. In this review, we provide an overview of the biological functions of RHAMM in non-neoplastic cells and cancer cells, as well as its association with CD44, and also introduce studies that particularly implicate RHAMM in the pathogenesis of head and neck cancers.
    Journal of Cancer Research and Clinical Oncology 03/2014; · 2.91 Impact Factor
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    ABSTRACT: Cells sorted from head and neck cancers on the basis of their high expression of CD44 have high potency for tumor initiation. These cells are also involved in epithelial to mesenchymal transition (EMT) and we have previously reported that cancer stem cells (CSCs) exist as two biologically distinct phenotypes. Both phenotypes are CD44(high) but whereas one is also ESA(high) and maintains epithelial characteristics, the other is ESA(low) , has mesenchymal characteristics and is migratory. Examining CD44-regulated signal pathways in these cells we show that CD44, and also RHAMM, act to inhibit phosphorylation of glycogen synthase kinase 3β (GSK3β) and that such inhibition reduces the formation of both "tumour spheres" and "holoclone" colonies, functional indicators of stemness. GSK3β inhibition also reduces the expression of stem cell markers such as Oct4, Sox2 and Nanog and up-regulates expression of the differentiation markers Calgranulin B and Involucrin in the CD44(high) /ESA(high) cell fraction. Transition of CSCs out of EMT and back to the epithelial CSC phenotype is induced by GSK3β knockdown. These results indicate that GSK3β plays a central role in determining and maintaining the phenotypes and behavior of CSCs in vitro and are likely to be involved in controlling the growth and spread of tumours in vivo.
    Stem Cells 05/2013; · 7.70 Impact Factor
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    ABSTRACT: In this study, we found that wounding of a confluent monolayer of squamous cell carcinoma (SCC) cells induced epithelial-mesenchymal transition (EMT) specifically at the edge of the wound. This process required the combined stimulation of TGFβ, TNFα and PDGF-D. Such a combined cytokine treatment of confluent monolayers of the cells upregulated the expression levels of Snail and Slug via PI3K. The PI3K downstream effector, AKT, was dispensable for the upregulation of Snail and Slug, but essential for enabling EMT in response to upregulation of Snail and Slug. In a pool of freshly prepared cells expressing exogenous Snail via a retroviral vector to avoid clonal effects, only 20% of the growing cells displayed the EMT phenotype. The population of cells undergoing EMT was diminished when the cells formed a confluent monolayer. However, upon wounding of the confluent monolayer, EMT was induced in the collectively migrating cells at the wound edge. Moreover, co-expression of a constitutively active AKT mutant with Snail increased the incidence of EMT concomitantly with the accelerated collective cell motility. Based on these findings, we conclude that the plasticity of Snail family-mediated EMT in SCC cells is regulated by the PI3K-AKT axis in response to the environmental condition. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.
    Journal of Cellular Biochemistry 03/2013; · 3.06 Impact Factor
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    ABSTRACT: Fibro-osseous lesions of the jaw are poorly understood because of a significant overlap of clinical, radiological and histological features among the various types, though they present distinct patterns of disease progression. An ossifying fibroma is associated with significant cosmetic and functional disturbances, as it shows expansive proliferation. Thus, it is important to establish a specific marker, as well as clearly elucidate its etiology for diagnosis and proper treatment. We previously established immortalized cell lines from human ossifying fibromas of the jaw and found that they highly expressed the receptor for hyaluronan (HA)-mediated motility (RHAMM). In this study, we examined the expression of RHAMM mRNA in 65 fibro-osseous lesions, including ossifying fibroma, fibrous dysplasia and osseous dysplasia, as well as 5 normal jaws, using real-time RT-PCR and immunohistochemistry assays. RHAMM mRNA and protein expression were significantly elevated in the ossifying fibroma specimens. These results suggest that detection of upregulated RHAMM expression in an ossifying fibroma assists with differential diagnosis and has a key role in elucidation of its pathophysiology.
    Histology and histopathology 02/2013; · 2.28 Impact Factor
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    ABSTRACT: BACKGROUND: Various instruments have been developed for collecting bone debris during intraoral autogenous bone graft procedures in implant surgery. The aim of this study was to quantitatively determine the degree of contamination in bone debris collected by different devices. METHODS: Twelve patients underwent autogenous bone collection using a bone chisel, bone scraper, trephine drill, and bone filter during bone augmentation surgery as a part of implant therapy, and the total bacterial count in bone debris collected by each was determined. RESULTS: Following anaerobic incubation, bacterial colony formation was found in all of the samples. The mean colony forming units (CFU)/g in samples collected by the trephine drill was found to be significantly lower than that of samples obtained with the other devices, while those values for samples collected by the bone scraper and bone filter was significantly higher as compared to the bone chisel and trephine drill CONCLUSION: The bacterial levels may still carry the infection risk. Thus prophylactic antibiotic therapy maybe indicated when using bone particles for intraoral augmentation procedures.
    Head & Face Medicine 01/2013; 9(1):3. · 0.98 Impact Factor
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    ABSTRACT: Oral keratinocytes and fibroblasts may be the first line of host defense against oral microorganisms. Here, we tested the hypothesis that oral keratinocytes and fibroblasts recognize microbial components via Toll-like receptors (TLRs) and participate in development of oral inflammation. Our results showed that immortalized oral keratinocytes (RT7), fibroblasts (GT1) and primary cells expressed mRNA of TLRs 1-10. Interleukin-8 (IL-8) production from RT7 cells was induced by treatment with TLR1-9 except for TLR7 agonist, while, GT1 cells were induced to produce IL-8 by all TLR agonists tested except for TLR7 and TLR9. GT1 cells showed increased CXCL10 production following treatment with agonists for TLR1/2, TLR3, TLR4 and TLR5, while only those for only TLR3 and TLR5 increased CXCL10 production in RT7 cells. Moreover, TLR agonists differentially regulated TNF-α-induced IL-8 and CXCL10 production by the tested cell types. These findings suggest that recognition of microorganism-derived pathogen in oral keratinocytes and fibroblasts by TLR may have important role to orchestrate host immune responses via production of various chemokines.
    Microbiology and Immunology 12/2012; · 1.55 Impact Factor
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    ABSTRACT: We previously identified genes associated with Snail-mediated squamous cell carcinoma (SCC) invasiveness, in which we observed significant elevation of Cyr61 expression. In this study, SCC cell lines overexpressing Cyr61 exhibited constitutive activation of Rho A and upregulated invasiveness without the disruption of hemophilic cell attachment. Humoral Cyr61 enhanced further production of endogenous Cyr61 by SCC cells, which stimulated collective cell migration and the development of an invasive tumor nest. We propose a Cyr61-dependent model for the development of invasive SCC nest, whereby a subset of tumor cells that highly produce Cyr61 may direct other tumor cells to undergo collective cell migration, resulting in a formation of primary SCC mass.
    Cancer letters 11/2012; · 5.02 Impact Factor
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    ABSTRACT: Objective: Involvement of epithelial-to-mesenchymal transition (EMT) in cancer invasion and metastasis has recently been highlighted. Stromal signals (e.g., TFGß) induce EMT with altered expression of epithelial and mesenchymal markers, changes in cellular morphology, and increased ability to migrate and invade. The EMT process induced in cancer cells at the margins of in vitro epithelial wounds was investigated as a model of the invasive tumour margin. Method: Control, and TGFß and TNFa-treated Ca1 cell populations, were examined to determine EMT levels. Cells cultured in medium with/without TGFß/TFGß-inhibitor were scraped to produce denuded areas and coverage by migrating cells, cell morphology, and vimentin and twist immunopositivity, examined. The EMT (CD44hi/ESAlow) and non-EMT (CD44hi/ESAhi) fractions of CSC were independently isolated, scratch-assayed and analysed. Result: Markedly increased EMT levels were induced by TGFß and TNFa, and reduced by specific inhibitors. After 12h, control cells showed migration of elongated, vimentin-positive cells into denuded areas, with their partial closure by 48h. TGFß-treatment led to a significant increase in the coverage of denuded areas at 24h (3-fold) compared to controls, and also to increased vimentin immunostaining. Conversely, coverage was lower when TGFß-inhibitor was added. Scratch assays of Ca1 cells FACS-sorted independently into EMT and non-EMT subpopulations showed co-staining of vimentin and twist, and this was higher for the EMT cells. Conclusion: In vitro assays provide consistent data for EMT changes occurring in the CSC fraction of OSCC. TGFß induction of higher expression of vimentin and twist in migrating cells, together with induction of higher motility and faster wound closure, confirm that the EMT process occurring in malignant cells is responsive to agents known to induce EMT in normal tissues and that such in vitro systems can provide suitable models for analysis of cytokine interactions during cancer invasion in vivo.
    IADR General Session 2012; 06/2012
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    ABSTRACT: Oral Diseases (2012) 18, 756-762 Objectives:  An odontoma, which shows proliferating odontogenic epithelium and mesenchymal tissue, is one of the most common odontogenic tumors encountered. These are commonly found in tooth-bearing regions, although the etiology remains unknown. There are no previous reports of an established line of immortalized human odontoma cells. Methods:  Using odontoma fragments obtained from a girl treated at our department, we established an immortalized human odontoma cell line and investigated cell morphology, dynamic proliferation, the presence of contamination, and karyotype. Moreover, cell characterization was examined using osteogenic and odontogenic markers. Results:  We successfully established a mesenchymal odontoma cell (mOd cells). The cells were found to be fibroblastic and had a high level of telomerase activity. Cell growth was confirmed after more than 200 population doublings without significant growth retardation. mOd cells expressed mRNA for differentiation markers, including collagen type I (COLI), alkaline phosphatase, bone sialoprotein, osteopontin, osteocalcin, cementum-derived protein (CP-23), dentin sialophosphoprotein (DSPP), and distal-less homeobox 3 (DLX3), as well as bone morphogenetic proteins (BMPs). In addition, they showed a high level of calcified nodule formation activity in vitro. Conclusions:  We successfully established a cell line that may be useful for investigating the mechanisms of normal odontogenesis as well as characteristics of odontoma tumors.
    Oral Diseases 04/2012; 18(8):756-762. · 2.38 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the clinical behavior and the histological aspects of interconnected porous hydroxyapatite ceramics (IP-CHA) in maxillary sinus floor augmentation procedures. A 59-year-old female patient received one-stage implant integration with right maxillary sinus floor augmentation with mixture grafts from the cortical bone and IP-CHA. Implant stability of each fixture increased at 9 months after fixture installation compared with the first operation and adequate fixation of each fixture could be obtained. Histological analysis revealed there was new bone formation in the majority of pores of IP-CHA. Moreover, on a panoramic radiograph taken at 33 months the mixture grafts were distinctly observed as a radiopacity in the right sinus cavity, and marked absorption of mixture grafts was not found. Our results suggest that IP-CHA has the potential to provide a major scaffold for osteoprogenitor cells and is a useful grafting material for maxillary sinus augmentation.
    Dental Materials Journal 02/2012; 31(1):54-60. · 0.81 Impact Factor
  • H Shigeishi, K Higashikawa, N Kamata
    Atlas of Genetics and Cytogenetics in Oncology and Haematology. 11/2011;
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    ABSTRACT: Receptor for hyaluronan (HA)-mediated motility (RHAMM) was first described as a soluble HA binding protein released by sub-confluent migrating cells. We previously found that RHAMM was highly expressed and plays an important role in proliferation in the human cementifying fibroma (HCF) cell line, which we previously established. HCF is a benign fibro-osseous neoplasm of the jaw and is composed of fibrous tissue containing varying amounts of mineralized material. However, the pathogenesis of HCF is not clear. In this paper, we examined the roles of RHAMM in osteoblastic cells. We generated RHAMM-overexpressing MC3T3-E1 cells and examined the cell proliferation and differentiation of osteoblastic cells. In MC3T3-E1 cells, overexpressing RHAMM was located intracellular and activated ERK1/2. Interestingly, the ERK1/2 activated by RHAMM overexpression promoted cell proliferation and suppressed the differentiation of osteoblastic cells. Our findings strongly suggest that RHAMM may play a key role in the osteoblastic differentiation process. The rupture of balance from differentiation to proliferation induced by RHAMM overexpression may link to the pathogenesis of bone neoplasms such as HCF.
    Journal of Bone and Mineral Metabolism 09/2011; 30(3):293-303. · 2.22 Impact Factor
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    ABSTRACT: Approximately 85% of human malignant tumors express increased levels of telomerase. The marked association of telomerase activity with malignant tissue provides strong evidence that telomerase activity is a significant marker for the diagnosis of cancer. In this study, telomerase activity was examined in 12 benign salivary gland tumors (8 pleomorphic adenomas and 4 adenolymphomas), 24 malignant tumors (15 mucoepidermoid carcinomas, 6 adenoid cystic carcinomas and 3 acinic cell carcinomas) and 6 non-neoplastic salivary glands. The mRNA expression of the human telomerase reverse transcriptase (hTERT) and additional telomerase‑associated proteins (hTEP1, p23, Hsp90 and dyskerin) was also examined. Of the 24 malignant tumors, 15 revealed strong telomerase activity. The non-neoplastic salivary glands appeared to have a negative telomerase expression. Furthermore, telomerase activity was significantly higher in high-grade mucoepidermoid carcinomas compared to low‑grade ones (Student's t-test, p<0.05). A significant correlation was found between telomerase activity and mRNA expression of hTERT in 15 cases, including non-neoplastic salivary glands and tumors (Spearman's rank correlation test, p<0.05). Furthermore, a significant correlation was found between telomerase activity and mRNA expression of EGFR (Spearman's rank correlation test, p<0.001). The results suggest that not only hTERT, but also EGFR play a significant role in the activation of telomerase. In conclusion, the results suggest that telomerase activity and hTERT/EGFR mRNA expression are useful markers for the detection of malignant cells in salivary gland carcinomas. Moreover, our results indicated that telomerase activity determines the degree of malignancy of mucoepidermoid carcinoma.
    Oncology letters 09/2011; 2(5):845-850. · 0.24 Impact Factor
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    ABSTRACT: We found a linear correlation between the Prostaglandin E(2) (PGE(2)) amount and the NR4A2 expression in oral squamous cell carcinoma (SCC) tissues through a statistical analysis among 41 clinical cases. In SCC cell lines, PGE(2) receptor (EP) ligation by exogenous PGE(2) promoted the NR4A2 expression in the cAMP/protein kinase A (PKA)-dependent manner. The process required a nature of SCC cell represented by constitutive activated epidermal growth factor receptor (EGFR) family. Targeted inactivation of the EGFRs interfered the PGE(2)-dependent NR4A2 expression. The PGE(2)-dependent NR4A2 induction is essential for the resistance to anti-cancer drug-induced apoptosis especially in SCC cells which showed constitutive EGFRs activity via autocrine epiregulin, a ligand for EGFRs. Conversely, SCC cells which lack epiregulin expression in their nature could gain the ability to promote the NR4A2 expression in response to PGE(2) and attain the resistance to anti-cancer drug-induced apoptosis under the existence of exogenous epiregulin. These findings suggest that susceptibility of SCC to anti-cancer drug could be compromised when PGE(2) was delivered in the microenvironment of SCC cells supported by constitutive EGFR family activities as their nature.
    Cancer letters 08/2011; 307(2):227-36. · 5.02 Impact Factor
  • Journal of oral and maxillofacial surgery: official journal of the American Association of Oral and Maxillofacial Surgeons 08/2011; 70(3):626-31. · 1.58 Impact Factor
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    ABSTRACT: We have previously established immortalized cells (HCF) from cementifying fibroma of the jaw bone. Here, we found that the receptor for hyaluronan (HA)-mediated motility (RHAMM) and epiregulin, a ligand for the epidermal growth factor receptor (EGFR), were highly expressed in HCF cells in comparison with osteoblasts by conducting a microarray analysis. The cell growth of HCF cells was significantly decreased by the knockdown of RHAMM using small interfering RNA (siRNA). RHAMM was associated with extracellular signal-regulated kinase (ERK) and essential for ERK phosphorylation. HCF cells had characteristic growth mechanisms in which epiregulin functions in an extracellular autocrine loop. Interestingly, exogenous HA induced the phosphorylation of EGFR, which was mainly dependent on CD44. The results raise the novel idea that the EGFR may activate Raf-MEK-ERK signaling in response to the binding of HA to CD44. Moreover, RHAMM was able to associate with TPX2 in the nucleus and was required for HA-induced activation of the Aurora A kinase. The results suggest that RHAMM has a predominant role in the cell cycle in HCF. Here, we report the new machinery by which RHAMM/ERK interaction induces the proliferative activity of cementifying fibroma cells via a specific signaling pathway through the CD44-EGFR axis.
    Laboratory Investigation 10/2010; 91(3):379-91. · 3.96 Impact Factor
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    ABSTRACT: Oral fibroblasts as well as keratinocytes are thought to influence host inflammatory responses against Candida albicans. However, little is known about chemokine expressions in oral fibroblasts against C. albicans infection. We therefore examined whether C. albicans induced several chemokines including fractalkine/CX3CL1 (CX3CL1), a unique chemokine that has properties of both chemoattractants and adhesion molecules, in fibroblasts and keratinocytes. The addition of C. albicans live cells to human immortalized oral keratinocytes (RT7) resulted in increases in the mRNA levels of multiple chemokines, but not of CX3CL1. In contrast, live and heat-killed C. albicans caused an increase in CX3CL1 mRNA and protein expression in human immortalized oral fibroblasts (GT1). CX3CL1 mRNA expression in GT1 cells was also enhanced by stimulation with a nonalbicans species of Candida. Further, the CX3CL1 chemokine domain showed antifungal activity against C. albicans. CX3CL1 secreted by oral fibroblasts appears to play an important role in the oral immune response to C. albicans infection.
    FEMS Immunology & Medical Microbiology 08/2010; 60(2):179-85. · 2.68 Impact Factor

Publication Stats

474 Citations
128.81 Total Impact Points

Institutions

  • 2013–2014
    • Queen Mary, University of London
      Londinium, England, United Kingdom
  • 2001–2014
    • Hiroshima University
      • • Department of Oral and Maxillofacial Surgery
      • • Faculty of Medicine
      Hirosima, Hiroshima, Japan
  • 2001–2002
    • Nara Medical University
      Kashihara, Nara, Japan