Biofilm formation in Staphylococcus implant infections. A review of molecular mechanisms and implications for biofilm-resistant materials.

Increasing attention has been focused on understanding bacterial biofilms and this growth modality's relation to human disease. In this review we explore the genetic regulation and molecular components involved in biofilm formation and maturation in the context of the Gram-positive cocci, Staphylococcus aureus. In addition, we discuss diseases and host immune responses, along with current therapies associated with S. aureus biofilm infections and prevention strategies.

https://www.tandfonline.com/doi/pdf/10.4161/viru.2.5.17724

Staphylococcus aureus biofilms: properties, regulation, and roles in human disease.

http://bioold.science.ku.dk/mkuhl/pages/PDF/Bjarnsholt%20et%20al%202013.pdf

The in vivo biofilm

Biofilms are complex communities of bacteria encased in a matrix composed primarily of polysaccharides, extracellular DNA, and protein. Staphylococcus aureus can form biofilm infections, which are often debilitating due to their chronicity and recalcitrance to antibiotic therapy. Currently, the immune mechanisms elicited during biofilm growth and their impact on bacterial clearance remain to be defined. We used a mouse model of catheter-associated biofilm infection to assess the functional importance of TLR2 and TLR9 in the host immune response during biofilm formation, because ligands for both receptors are present within the biofilm. Interestingly, neither TLR2 nor TLR9 impacted bacterial density or inflammatory mediator secretion during biofilm growth in vivo, suggesting that S. aureus biofilms circumvent these traditional bacterial recognition pathways. Several potential mechanisms were identified to account for biofilm evasion of innate immunity, including significant reductions in IL-1β, TNF-α, CXCL2, and CCL2 expression during biofilm infection compared with the wound healing response elicited by sterile catheters, limited macrophage invasion into biofilms in vivo, and a skewing of the immune response away from a microbicidal phenotype as evidenced by decreases in inducible NO synthase expression concomitant with robust arginase-1 induction. Coculture studies of macrophages with S. aureus biofilms in vitro revealed that macrophages successful at biofilm invasion displayed limited phagocytosis and gene expression patterns reminiscent of alternatively activated M2 macrophages. Collectively, these findings demonstrate that S. aureus biofilms are capable of attenuating traditional host proinflammatory responses, which may explain why biofilm infections persist in an immunocompetent host.

/pdf/staphylococcus-aureus-biofilms-prevent-macrophage-3c6zrqx02z.pdf

Staphylococcus aureus Biofilms Prevent Macrophage Phagocytosis and Attenuate Inflammation In Vivo

The staphylococci comprise a diverse genus of Gram-positive, nonmotile commensal organisms that inhabit the skin and mucous membranes of humans and other mammals. In general, staphylococci are benign members of the natural flora, but many species have the capacity to be opportunistic pathogens, mainly infecting individuals who have medical device implants or are otherwise immunocompromised. Staphylococcus aureus and Staphylococcus epidermidis are major sources of hospital-acquired infections and are the most common causes of surgical site infections and medical device-associated bloodstream infections. The ability of staphylococci to form biofilms in vivo makes them highly resistant to chemotherapeutics and leads to chronic diseases. These biofilm infections include osteomyelitis, endocarditis, medical device infections, and persistence in the cystic fibrosis lung. Here, we provide a comprehensive analysis of our current understanding of staphylococcal biofilm formation, with an emphasis on adhesins and regulation, while also addressing how staphylococcal biofilms interact with the immune system. On the whole, this review will provide a thorough picture of biofilm formation of the staphylococcus genus and how this mode of growth impacts the host.

The Staphylococcal Biofilm: Adhesins, Regulation, and Host Response.

http://www.endoexperience.com/documents/Guentheretal2009PMNsBiofilm.pdf

Host defence against Staphylococcus aureus biofilms infection: phagocytosis of biofilms by polymorphonuclear neutrophils (PMN).

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.

Destruction of bacterial biofilms by polymorphonuclear neutrophils: relative contribution of phagocytosis, DNA release, and degranulation.

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 H-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.

Phagocytosis of staphylococci biofilms by polymorphonuclear neutrophils: S. aureus and S. epidermidis differ with regard to their susceptibility towards the host defense.

Host defence against Staphylococcus aureus biofilms by polymorphonuclear neutrophils: Oxygen radical production but not phagocytosis depends on opsonisation with immunoglobulin G

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Host defence against Staphylococcus aureus biofilms infection: phagocytosis of biofilms by polymorphonuclear neutrophils (PMN).

Destruction of bacterial biofilms by polymorphonuclear neutrophils: relative contribution of phagocytosis, DNA release, and degranulation.

Phagocytosis of staphylococci biofilms by polymorphonuclear neutrophils: S. aureus and S. epidermidis differ with regard to their susceptibility towards the host defense.

Host defence against Staphylococcus aureus biofilms by polymorphonuclear neutrophils: Oxygen radical production but not phagocytosis depends on opsonisation with immunoglobulin G