Biofilm matrix

About: Biofilm matrix is a research topic. Over the lifetime, 1589 publications have been published within this topic receiving 110140 citations.

Medical significance and new therapeutical strategies for biofilm associated infections

Abstract: Recent public announcements stated that 60% to 85% of all microbial infections involve biofilms developed on natural tissues (skin, mucosa, endothelial epithelia, teeth, bones) or artificial devices (central venous, peritoneal and urinary catheters, dental materials, cardiac valves, intrauterine contraceptive devices, contact lenses, different types of implants). Prosthetic medical devices are risk factors of chronic infections in developed countries and these infections are characterized by slow onset, middle intensity symptoms, chronic evolution and resistance to antibiotic treatment. In case of biofilm development, a series of genes (40-60% of the prokaryotic genome) are modulated (activated/inhibited) by complex cell to cell signalling mechanisms and the biofilm cells become phenotypically distinct from their counterpart--free cells, being more resistant to stress conditions (including all types of antimicrobial substances); this resistance is phenotypical, behavioural and, more recently, called TOLERANCE. Four major mechanisms can account for biofilm antibiotic tolerance: (1) the failure of antibiotic penetration into the depth of a mature biofilm due to the biofilm matrix; (2) the accumulation of high levels of antibiotic degrading enzymes; (3) in the depth of biofilm, cells are experiencing nutrient limitation entering in a slow-growing or starved state; slow-growing or non-growing cells being not highly susceptible to antimicrobial agents, this phenomenon could be amplified by the presence of phenotypic variants or "persisters" and (4) biofilm's bacteria can turn on stress-response genes and switch to more tolerant phenotypes on exposure to environmental stresses; (5) genetic changes, probably selected by different stress conditions, such as mutations and gene transfer could occur inside the biofilm. In these conditions, biofilm associated infections require a different approach, both clinically and paraclinically.

Extracellular Polymers in Biofilms

Abstract: Many of those who study biofilms view them as a collection of living organisms at an interface but this definition should be expanded to include the products of those organisms. A major product is the matrix in which biofilm cells are found. It is somewhat surprising that there is such an emphasis on the biotic component of the film because this phase occupies only a small fraction of the volume (Characklis & Cooksey, 1983). It is often the biofilm matrix that causes many of the economic problems associated with biofilm formation since it acts as a layer of immobilized water. It is in fact highly hydrated and contains 98–99% water (Christensen and Characklis, 1990). This matrix, which is really a collection of polymers rather than a single material, is made by many organisms in biofilms. The polymers have been referred to collectively as capsules, sheaths, slime and glycocalyces. Costerton et al (1981) proposed the term glycocalyx for use in procaryotic biology. They defined a glycocalyx as “those polysaccharide-containing structures of bacterial origin, lying outside the integral elements of the outer membrane of Gram-negative cells and the peptidoglycan of Gram-positive cells”. They further subdivided glycocalyces into (1) glycoprotein subunits at the cell surface and (2) capsules. “Capsules” were further subdivided into (a) those that are rigid and exclude particles such as Indian ink ( a classical negative “stain” in bacteriology); (b) those, which in contrast to (a), are flexible and include Indian ink; (c) integral capsules that are closely associated with the cell surface and (d) those capsules that are peripheral to the cell and can be lost to the aqueous phase. In a brief but comprehensive review (Geesey, 1982), Geesey used a less structured term for the high molecular weight material extracellular to cells.

Staphylokinase Control of Staphylococcus aureus Biofilm Formation and Detachment Through Host Plasminogen Activation

Abstract: Staphylococcus aureus biofilms, a leading cause of persistent infections, are highly resistant to immune defenses and antimicrobial therapies. In the present study, we investigated the contribution of fibrin and staphylokinase (Sak) to biofilm formation. In both clinical S. aureus isolates and laboratory strains, high Sak-producing strains formed less biofilm than strains that lacked Sak, suggesting that Sak prevents biofilm formation. In addition, Sak induced detachment of mature biofilms. This effect depended on plasminogen activation by Sak. Host-derived fibrin, the main substrate cleaved by Sak-activated plasminogen, was a major component of biofilm matrix, and dissolution of this fibrin scaffold greatly increased susceptibility of biofilms to antibiotics and neutrophil phagocytosis. Sak also attenuated biofilm-associated catheter infections in mouse models. In conclusion, our results reveal a novel role for Sak-induced plasminogen activation that prevents S. aureus biofilm formation and induces detachment of existing biofilms through proteolytic cleavage of biofilm matrix components.