Publicação
Dysbiotic biofilms increase the inflammatory response in periodontitis
| Resumo: | Periodontal diseases are perhaps the most common chronic inflammatory diseases in humans. Their main cause is the inflammatory destruction of the tooth-supporting (periodontal) tissues, as a result of bacterial colonization of the tooth, in the form of polymicrobial biofilm communities. An imbalance in the periodontal microbiota and dysbiosis deregulate the host immune response, leading to chronic inflammation. Since little is known about the initiation of dysbiosis, it can be hypothesized that some commensal bacteria can suppress the outgrowth of pathobionts by H2O2 production. However, serum and blood components released during inflammation can neutralize this suppressive effect, leading to the initiation of dysbiosis. The aim of this study is to determine if the neutralizing effect of serum, hemoglobin, hemin and peroxidase on the inhibitory effect of the commensal bacteria on pathobiont growth is translated in a more pronounced immune response. Bacterial quantitative PCR, cellular inflammatory genes and cytokine quantification, by ELISA, were performed to evaluate the pathobiont outgrowth and to detect possible differences in the inflammatory response after exposure of cell cultures to homeostatic or dysbiotic biofilms. Peroxidases, serum and blood components neutralized the inhibitory effect of H2O2 by exogenous peroxidase activity, increasing the pathobiont outgrowth. Exposure of epithelial and fibroblast cultures to these dysbiotic biofilms increased the expression of IL6, IL1β, TNFα, MMP1, MMP2, MMP8, HBD but especially of IL8. Moreover, higher amounts of IL8 were produced after the challenge with dysbiotic biofilms. Conversely, homeostatic and commensal biofilms had a minor inflammatory response at expression and protein level. Overall, serum, peroxidases or blood compounds allowed the outgrowth of pathobionts. Dysbiotic biofilms enriched in pathobionts significantly increased the inflammatory response compared to homeostatic and commensal biofilms. |
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| Autores principais: | Fernandes, Sara Raquel Matos |
| Assunto: | Periodontitis Oral biofilms Dysbiosis Immune response Periodontite Biofilmes orais Disbiose Resposta imunitária |
| Ano: | 2017 |
| País: | Portugal |
| Tipo de documento: | dissertação de mestrado |
| Tipo de acesso: | acesso restrito |
| Instituição associada: | Universidade do Minho |
| Idioma: | inglês |
| Origem: | RepositóriUM - Universidade do Minho |
| Resumo: | Periodontal diseases are perhaps the most common chronic inflammatory diseases in humans. Their main cause is the inflammatory destruction of the tooth-supporting (periodontal) tissues, as a result of bacterial colonization of the tooth, in the form of polymicrobial biofilm communities. An imbalance in the periodontal microbiota and dysbiosis deregulate the host immune response, leading to chronic inflammation. Since little is known about the initiation of dysbiosis, it can be hypothesized that some commensal bacteria can suppress the outgrowth of pathobionts by H2O2 production. However, serum and blood components released during inflammation can neutralize this suppressive effect, leading to the initiation of dysbiosis. The aim of this study is to determine if the neutralizing effect of serum, hemoglobin, hemin and peroxidase on the inhibitory effect of the commensal bacteria on pathobiont growth is translated in a more pronounced immune response. Bacterial quantitative PCR, cellular inflammatory genes and cytokine quantification, by ELISA, were performed to evaluate the pathobiont outgrowth and to detect possible differences in the inflammatory response after exposure of cell cultures to homeostatic or dysbiotic biofilms. Peroxidases, serum and blood components neutralized the inhibitory effect of H2O2 by exogenous peroxidase activity, increasing the pathobiont outgrowth. Exposure of epithelial and fibroblast cultures to these dysbiotic biofilms increased the expression of IL6, IL1β, TNFα, MMP1, MMP2, MMP8, HBD but especially of IL8. Moreover, higher amounts of IL8 were produced after the challenge with dysbiotic biofilms. Conversely, homeostatic and commensal biofilms had a minor inflammatory response at expression and protein level. Overall, serum, peroxidases or blood compounds allowed the outgrowth of pathobionts. Dysbiotic biofilms enriched in pathobionts significantly increased the inflammatory response compared to homeostatic and commensal biofilms. |
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