Combined influence of nitric oxide and surface roughness in biofilm reduction across bacteria strains

Effective use of medical device implants is often hindered by infection, which may cause the device to be rejected from the body and seriously endanger health. Such infections are often a result of biofilm formation or microbial colonies collecting on a surface. Therefore, a challenge in the medical field is to mitigate the impact of biofilm formation in order to save thousands of lives and millions of healthcare dollars annually. The proposed strategy is to target the attachment phase of the biofilm lifecycle to try to prevent the formation of antimicrobial resistant biofilms. Prevention of bacterial attachment may be induced through the introduction of nitric oxide (NO), a small biological signaling molecule known for its antibacterial properties. NO may be delivered via release from a donating molecule incorporated in the polymer composing the medical device. The NO donor S-nitrosoglutathione (GSNO) was utilized in this study because it is a relatively stable small molecule that naturally exists in the body, therefore negating possible adverse reactions when it is introduced to the body. Tygon^®, a polymer commonly found in Food and Drug Administration approved medical devices such as catheters, was utilized as a platform for the inhibition of biofilms. To study the necessary amount of released NO needed to cause a reduction in attachment across varying strains, different concentrations of GSNO were applied. Two Gram-negative (Pseudomonas aeruginosa and Acinetobacter baumannii) and two Gram-positive species (Staphylococcus aureus and Methicillin Resistant Staphylococcus aureus), all strong biofilm formers listed as urgent threats by the Center for Disease Control, illustrated different responses to NO. Gram-positive species showed a decrease in viability over 80% with an average total NO release of 2.01 ± 2.11 × 10 ^{-  4}μmols, while Gram-negative response was less, with viability decreasing to 38% (P. aeruginosa) and 71% (A. baumannii) with 1.25 ± 1.63 × 10^-4μmols NO. Further studies utilizing glutathione surface roughness controls highlight that increasing the surface roughness of the polymer platform produces no statistically significant difference in viability compared to the Tygon-only negative control in all strains except P. aeruginosa. Developing a quantitative understanding of how NO release and platform surface roughness impact biofilm attachment across Gram strains is key to reducing the incidence and impact of medical device associated infections.