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Bacteria organized in biofilms are a common cause of relapsing or persistent infections, and the ultimate cause of implant-associated osteomyelitis. In these patients, biofilms of staphylococci are prevalent. Bacteria organized as biofilms are relatively resistant towards antibiotics and biocides, and it is also assumed that they may escape host defense mechanisms. In this context, we have studied how polymorphonuclear neutrophils (PMN), the "first line of defense" against bacterial infection, interact with biofilms generated in vitro. We found that PMN recognize biofilms and activate defense-associated reactions, including phagocytosis, degranulation of lactoferrin and elastase, and DNA release as well. Destruction of biofilms ensues, showing that biofilms are not inherently protected against the attack by phagocytic cells.

Bacteria organized in biofilms are a common cause of relapsing or persistent infections. In patients receiving orthopedic implants, such as endoprostheses or osteosynthesis materials, Staphylococcus aureus and S. epidermidis are prevalent and it is widely assumed that bacteria in biofilms are not only relatively resistant towards antibiotics and biocides, but also towards host defense mechanisms. In that context, we addressed the question how polymorphonuclear neutrophils (PMN), the “first line defense” against bacterial infection, interact with biofilms generated in vitro. By time-lapse video microscopy, we observed migration of PMN towards the biofilms. In the case of S. aureus, the PMN moved across the biofilm and took up bacteria as they moved along. On S. epidermidis, in contrast, the PMN were rather immobile, and phagocytosis was limited to bacteria in the immediate vicinity. By labeling the bacteria within the biofilm with 3H-thymidine we found that S. aureus biofilms were more sensitive towards the PMN attack than S. epidermidis. Following phagocytosis of either bacteria strain, the PMN underwent apoptosis, in line with the dogma, that phagocytosis induces programmed cell-death in order to prevent spilling of the bactericidal and cytotoxic entities. In conclusion, biofilms are not inherently protected against the attack by phagocytic cells; their sensitivity, however, varies among bacterial strains, presumably due to properties of the extracellular biofilm matrix affecting the motility of PMN on the film.

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