The role of hyperglycemia in mechanisms of exacerbated inflammatory responses within the oral cavity
| Autor: | Matthew Waite, Jamie Amir, Shannon M. Wallet, Joseph Katz, Jeffrey Tobler, Dana L. Catalfamo, Theofilos Koutouzis |
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| Rok vydání: | 2011 |
| Předmět: |
Adult
Male Lipopolysaccharide endocrine system diseases Adolescent Receptor expression Immunology Primary Cell Culture Receptor for Advanced Glycation End Products Inflammation Biology Ligands Article RAGE (receptor) chemistry.chemical_compound Immune system medicine Humans Receptors Immunologic Immunity Mucosal Aged Mouth Innate immune system nutritional and metabolic diseases Epithelial Cells Receptor Cross-Talk Middle Aged Immunity Innate Toll-Like Receptor 4 chemistry Mucosal immunology Diabetes Mellitus Type 2 Case-Control Studies Hyperglycemia Chronic Periodontitis TLR4 Female medicine.symptom Signal Transduction |
| Zdroj: | Cellular immunology. 272(1) |
| ISSN: | 1090-2163 |
| Popis: | Immune modulating factors are necessary for pathogen clearance, but also contribute to host tissues damage, as those seen in periodontal diseases. Many of these responses can be exacerbated by host conditions including type 2 diabetes [T2D], where toll-like receptor 4 [TLR4] and the receptor for advanced glycated end products [RAGE] play a significant role. Here we investigate causality associated with the increase in inflammatory markers observed in periodontally diseased patients with T2D using multi-variant correlation analysis. Inflammation associated with periodontal diseases, characterized by elevated pro-inflammatory cytokines, innate immune receptor expression, and cellular infiltrate was exacerbated in patients with T2D. In addition, a feed forward loop regulated by poor glycemic control was associated with a loss of mucosal barrier integrity and accumulation of innate immune receptor ligands resulting in an exacerbation of ongoing inflammation, where RAGE and TLR4 cooperated to induce responses in oral epithelial cells, which were exacerbated by hyperglycemia. |
| Databáze: | OpenAIRE |
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