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Stromal-Epithelial Cytokine Crosstalk in Experimentally Induced Periodontal Disease
Firth JD1*, Ekuni D2, Putnins EE3
1Department of Oral Biological & Medical Sciences, Faculty of Dentistry, The University of British Columbia, Vancouver, Canada; 2Preventive Dentistry & Pathology & Pathobiology, Okayama University Graduate School of Medicine, Dentistry & Pharmaceutical Sciences, Okayama, Japan
Objectives: Lipopolysaccharide (LPS) is a bacterial virulence factor implicated in the conversion of junctional to pocket epithelium, an early marker of periodontal disease onset. During disease progression, the epithelial barrier is compromised, allowing virulence factors to insult underlying stroma. We sought to determine if LPS-induced changes in diffusible gene products could affect signaling crosstalk between stromal and epithelial tissues, contributing to disease.
Methods: Wistar strain rats (14 male) were divided between time 0 control and 8-week treatment groups. LPS was applied daily into the gingival sulcus and histological analysis confirmed the onset of disease. Junctional epithelium and underlying stromal tissue was separately collected from healthy and diseased animals by laser-capture micro-dissection and subject to gene expression microarray analysis. Genmapp bioinformatic analysis was performed to identify gene ontology function groups of high significance (z>4) whose protein products could potentially interact. In vitro validation used a chronic wound cell culture model and protein analysis by flow cytometry.
Results: LPS-altered gene ontology function grouping top-ranked the molecular binding category in both epithelia and stromal tissues. However, for stroma, the cytokine subgroup ranked near the top (z=5.991). Its three top-ranked stromal genes (amphiregulin, interleukin 1-β, and Fas ligand) are known to be diffusible and capable of modulating the epithelial growth factor (EGF) pathway. For epithelia, several binding subgroups associated with the EGF receptor were highly ranked, including ErbB-2 class receptor binding (z=4.994). Its top three altered genes (Fos ligand, mucin 4, and somatostatin receptor) were downregulated. All are reported as playing a role in normally inhibiting EGF signaling. Upregulation of all 3 stromal and downregulation of all 3 epithelial gene products was confirmed in vitro for up to 3 weeks with LPS treatment.
Conclusions: LPS may contribute to the onset of periodontitis by upregulating EGF pathway activity via stromal-epithelial crosstalk.
Acknowledgements: Supported by Canadian Institutes of Health Research grant MOP-82830 to EEP.