As referred before, the molecular mechanism underlying S. epidermidis biofilm formation has been extensively studied in the last years. However, when it comes to the interaction of biofilms with the host immune system effectors very little is known.
In this manuscript the authors aimed to understand the interaction between the S. epidermidis extracellular matrix and the potent phagocytic polymorphonuclear cells (PMNs). An effective phagocytic process by PMNs depends on the opsonization of the antigen by complement proteins and IgG. However, previous work developed by these authors has shown that PMNs are activated in the presence of S. epidermidis biofilms and start the phagocytic process even in the absence of opsonins, indicating that some of the biofilm matrix components may stimulate PMNs activation.
Therefore, in this study the characterization of PMNs activation by non-opsonized S. epidermidis biofilms and purified matrix fractions was performed.
Interestingly, it was observed that some proteins purified from the matrix were able to up-regulate activation receptors such as CD11b, CD18 and CD66b present in PMNs cells. Additionally, PMNs activation was also assessed by the release of lactoferrin. Both non-opsonized biofilms and protein purified fractions from the matrix were able to induce lactoferrin release. However, elastase release, another factor produced by activated PMNs, was dependent on the opsonization and therefore, the components of non-opsonized S. epidermidis biofilms or protein fractions of the matrix were not able to induce elastase release.
Moreover, independently of the opsonization of the biofilms, neutrophils extracellular traps (NETs) that bind the antigen were stimulated . Nevertheless, protein fractions purified from the matrix were not able to induce NETs release indicating that there are other activation signals involved in the process of PMNs activation.
Taken together these results provide evidence that some S. epidermidis biofilms matrix components are able to activate PMNs. However other signaling pathways are involved since some of the activation signals of PMNs are only produced when in contact with intact biofilms.
Is thus clear that S. epidermidis biofilms are not inherently protected against host defense mechanisms which has to be explored in order to find ways to avoid biofilm formation in indwelling medical devices and all the serious biofilm-related infections associated.
Reference of the paper summarized above:
Meyle E, Brenner-Weiss G, Obst U, Prior B, Hänsch GM. (2012) “Immune defense against S. epidermidis biofilms: components of the extracellular polymeric substance activate distinct bactericidal ?mechanisms of phagocytic cells.” Int J Artif Organs: 35(10):700-12.
RM: AF 1399