Abstract

RATIONALE: Bacterial biofilms are known entities in chronic rhinosinusitis (CRS) and have recently been correlated with post therapeutic persistent inflammation and recalcitrant disease. Thus, we set out to determine whether sinonasal mucosal biofilms alter the local inflammatory response in CRS.METHODS: Sinonasal mucosa was collected during surgery from 23 consented, steroid naïve, adult CRS patients and 16 control patients. Biofilm presence on the mucosa was determined using SEM. Leukocytes extracted from the mucosa underwent FACS analysis for granulocytes, neutrophils and eosinophils, and B cells using fluorescently tagged antibodies to CD15, CD16, and CD19, respectively. IL-8 was measured from homogenized tissue lysate using a Procarta luminex cytokine assay.RESULTS: 4 out of 12 control patients and 5 out of 18 CRS patients had definitive biofilms. A student's t-test revealed significantly (P < 0.05) elevated levels of neutrophils, B cells, and IL-8 in the biofilm-positive CRS patients compared to the biofilm-negative CRS patients. The only significant difference found in the control subgroups was a decrease in granulocytes in the biofilm-positive patients.CONCLUSIONS: Biofilms stimulate a unique and ineffective immune response compared to non-biofilm mediated CRS. Further investigation into the host response to biofilms may provide insight into novel therapeutic strategies for the management of biofilm induced inflammatory diseases such as chronic rhinosinusitis. RATIONALE: Bacterial biofilms are known entities in chronic rhinosinusitis (CRS) and have recently been correlated with post therapeutic persistent inflammation and recalcitrant disease. Thus, we set out to determine whether sinonasal mucosal biofilms alter the local inflammatory response in CRS. METHODS: Sinonasal mucosa was collected during surgery from 23 consented, steroid naïve, adult CRS patients and 16 control patients. Biofilm presence on the mucosa was determined using SEM. Leukocytes extracted from the mucosa underwent FACS analysis for granulocytes, neutrophils and eosinophils, and B cells using fluorescently tagged antibodies to CD15, CD16, and CD19, respectively. IL-8 was measured from homogenized tissue lysate using a Procarta luminex cytokine assay. RESULTS: 4 out of 12 control patients and 5 out of 18 CRS patients had definitive biofilms. A student's t-test revealed significantly (P < 0.05) elevated levels of neutrophils, B cells, and IL-8 in the biofilm-positive CRS patients compared to the biofilm-negative CRS patients. The only significant difference found in the control subgroups was a decrease in granulocytes in the biofilm-positive patients. CONCLUSIONS: Biofilms stimulate a unique and ineffective immune response compared to non-biofilm mediated CRS. Further investigation into the host response to biofilms may provide insight into novel therapeutic strategies for the management of biofilm induced inflammatory diseases such as chronic rhinosinusitis.

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