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Disrupting the biofilm matrix improves wound healing outcomes

02 February 2019
Volume 3 · Issue 1



The most unyielding molecular component of biofilm communities is the matrix structure that it can create around the individual microbes that constitute the biofilm. The type of polymeric substances (polymeric sugars, bacterial proteins, bacterial DNA and even co-opted host substances) are dependent on the microbial species present within the biofilm. The extracellular polymeric substances that make up the matrix give the wound biofilm incredible colony defences against host immunity, host healing and wound care treatments. This polymeric slime layer, which is secreted by bacteria, encases the population of microbes, creating a physical barrier that limits the ingress of treatment agents to the bacteria. The aim of this study was to determine if degrading the wound biofilm matrix would improve wound healing outcomes and if so, if there was a synergy between treating agents that disrupted biofilm defenses with Next Science BlastX Antimicrobial Wound Gel (wound gel) and cidal agents (topical antibiotics).


A three-armed randomised controlled trial was designed to determine if standard of care (SOC) was superior to SOC plus wound gel (SOC + gel) and wound gel alone. The wound gel used in this study contains components that directly attack the biofilm extracellular polymeric substance. The gel was applied directly to the wound bed on a Monday–Wednesday–Friday interval, either alone or with SOC topical antibiotics.


Using a surrogate endpoint of 50% reduction in wound volume, the results showed that SOC healed at 53%, wound gel healed at 80%, while SOC plus wound gel showed 93% of wounds being successfully treated.


By directly targeting the wound biofilm matrix, wound healing outcomes are improved.

Chronic wounds, regardless of the aetiology, exhibit similar clinical behaviours, such as stalled healing and exudate production, which are directly related to microorganisms on the wound surface growing as a biofilm.1 It is now widely recognised that all chronic infections are produced by microorganisms in the biofilm mode of growth.2,3 How biofilm produces a host infection is now well defined at a molecular, cellular and clinical level.4

There are countless molecular strategies used by bacteria, yeast and fungus to produce host infection, which we see clinically as chronic infection.5,6 Of the subcellular pathways employed by biofilm, four areas of research hold great promise for wound care. The first is how and why microbes express adhesins, surface complexes that target host tissues, to allow them to attach to a host environment.7 Second is the vast array of communication molecules (quorum sensing) produced by different species of microbes to organise the activity of the entire biofilm.8,9 Third is the amazing variety of ‘effectors’ (small proteins), which bacteria can secrete from a number of different secretory systems (for example, T3SS and T6SS), which take over the function of the wound bed cells.6,10 By producing cellular senescence, with these effectors, the biofilm establishes a stable attachment site from which to continue its persistent infection.

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