Abstract Title

Investigation of biofilm interference in macrophage-mediated immune defense against Staphylococcus aureus

Abstract

S. aureus biofilm infections, common in patients with chronic wounds or artificial implants, are clinically significant due to their ability to subvert the human innate immune response, especially through disruption of macrophage behavior. Previous investigations suggest that S. aureus biofilms attenuate macrophage inflammation by disrupting NF-κβ-coordinated transcription of iNOS, IL-6 and IL-1β. However, the primary mechanism by which this disruption occurs is not yet known. This study seeks to investigate two potential biofilm-mediated disturbances in the intracellular signaling pathway by synthetically polarizing M1 macrophages via stimulation of either Nod2 or TLR2, two known initiators of the NF-κβ activation pathway. Subsequent co-culture with biofilm conditioned media exposes these treated cells to biofilm components known to disrupt this process. Quantification of any changes in inflammatory macrophage behavior via qPCR and nitric oxide (NO) assays can help identify Nod2 or TLR2 pathways as dysfunctional in biofilm-related infections. Insight into this mechanism can lead to a better understanding of both the innate immune response to pathogens as well as to the development of new antimicrobial therapies to treat antibiotic-resistant biofilm infections.

Modified Abstract

S. aureus biofilm infections, common in patients with artificial implants, are clinically significant due to their ability to subvert the human innate immune response through disruption of macrophage behavior. S. aureus biofilms attenuate macrophage inflammation by disrupting NF-κβ-coordinated transcription of downstream cytokines. However, the primary mechanism by which this disruption occurs is not known. This study seeks to investigate two potential biofilm-mediated disturbances in the intracellular signaling pathway by utilizing an in vitro biofilm co-culture model to induce changes in macrophage behavior. These changes, quantified by qPCR and nitric oxide (NO) assays, can help identify dysfunctional pathways for further study. Insight into this mechanism can lead to a better understanding of the innate immune response and the development of antimicrobial therapies to treat antibiotic-resistant infections.

Research Category

Biomedical Sciences

Author Information

Tara RogersFollow

Primary Author's Major

Biology

Mentor #1 Information

Dr. Min-Ho Kim

Presentation Format

Poster

Start Date

5-4-2018 1:00 PM

Research Area

Biology | Cell and Developmental Biology | Immunology and Infectious Disease

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Apr 5th, 1:00 PM

Investigation of biofilm interference in macrophage-mediated immune defense against Staphylococcus aureus

S. aureus biofilm infections, common in patients with chronic wounds or artificial implants, are clinically significant due to their ability to subvert the human innate immune response, especially through disruption of macrophage behavior. Previous investigations suggest that S. aureus biofilms attenuate macrophage inflammation by disrupting NF-κβ-coordinated transcription of iNOS, IL-6 and IL-1β. However, the primary mechanism by which this disruption occurs is not yet known. This study seeks to investigate two potential biofilm-mediated disturbances in the intracellular signaling pathway by synthetically polarizing M1 macrophages via stimulation of either Nod2 or TLR2, two known initiators of the NF-κβ activation pathway. Subsequent co-culture with biofilm conditioned media exposes these treated cells to biofilm components known to disrupt this process. Quantification of any changes in inflammatory macrophage behavior via qPCR and nitric oxide (NO) assays can help identify Nod2 or TLR2 pathways as dysfunctional in biofilm-related infections. Insight into this mechanism can lead to a better understanding of both the innate immune response to pathogens as well as to the development of new antimicrobial therapies to treat antibiotic-resistant biofilm infections.