Sub-inhibitory tigecycline concentrations induce extracellular matrix binding protein Embp dependent Staphylococcus epidermidis biofilm formation and immune evasion

Weiser, Julian; Henke, Hanae A; Hector, Nina; Both, Anna; Martin, Coralie; Büttner, Henning; Kaplan, Jeffery B; Rohde, Holger

doi:10.1016/j.ijmm.2016.05.015

Cited by 28 publications

(27 citation statements)

References 58 publications

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“…Findings have also shown that the exopolymer limits the ability of leukocytes to penetrate the biofilm [ 32 ], hampers their movement through biofilms, attenuates their ability to degranulate and produce reactive oxygen species (ROS), and prevents the phagocytosis of bacteria [ 31 , 35 ]. Exposing bacterial biofilms to sub-inhibitory antibiotic concentrations, or to the wrong antibiotics, may induce mucoid phenotypes, which generate thicker biofilms with additional matrix components [ 36 , 37 , 38 ].…”

Section: Biofilm Resistancementioning

confidence: 99%

Microbial Biofilms and Chronic Wounds

Omar¹,

Wright²,

et al. 2017

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Background is provided on biofilms, including their formation, tolerance mechanisms, structure, and morphology within the context of chronic wounds. The features of biofilms in chronic wounds are discussed in detail, as is the impact of biofilm on wound chronicity. Difficulties associated with the use of standard susceptibility tests (minimum inhibitory concentrations or MICs) to determine appropriate treatment regimens for, or develop new treatments for use in, chronic wounds are discussed, with alternate test methods specific to biofilms being recommended. Animal models appropriate for evaluating biofilm treatments are also described. Current and potential future therapies for treatment of biofilm-containing chronic wounds, including probiotic therapy, virulence attenuation, biofilm phenotype expression attenuation, immune response suppression, and aggressive debridement combined with antimicrobial dressings, are described.

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Section: Biofilm Resistancementioning

confidence: 99%

Microbial Biofilms and Chronic Wounds

Omar¹,

Wright²,

et al. 2017

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“…All primers and probes were synthesized by MWG Eurofins, Germany. Cycling and subsequent analysis of qPCR data was performed as described previously (Weiser et al, 2016). Values were assumed to be normally distributed and the two-tailed Student's t-test was performed with the significance level set to 0.017 to account for multiple testing.…”

Section: Quantification Of Sepa Ecp and Esp Expressionmentioning

confidence: 99%

The metalloprotease SepA governs processing of accumulation‐associated protein and shapes intercellular adhesive surface properties in Staphylococcus epidermidis

Paharik

Kotasińska

Both

et al. 2017

Molecular Microbiology

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Summary The otherwise harmless skin inhabitant Staphylococcus epidermidis is a major cause of healthcare-associated medical device infections. The species' selective pathogenic potential depends on its production of surface adherent biofilms. Cell wall-anchored protein Aap promotes biofilm formation in S. epidermidis, independently from the polysaccharide intercellular adhesin PIA. Aap requires proteolytic cleavage to act as an intercellular adhesin. Whether and which staphylococcal proteases account for Aap processing is yet unknown. Here, evidence is provided that in PIA-negative S. epidermidis 1457Δica, the metalloprotease SepA is required for Aap-dependent S. epidermidis biofilm formation in static and dynamic biofilm models. qRT-PCR and protease activity assays demonstrated that under standard growth conditions, sepA is repressed by the global regulator SarA. Inactivation of sarA increased SepA production, and in turn augmented biofilm formation. Genetic and biochemical analyses demonstrated that SepA-related induction of biofilm accumulation resulted from enhanced Aap processing. Studies using recombinant proteins demonstrated that SepA is able to cleave the A domain of Aap at residue 335 and between the A and B domains at residue 601. This study identifies the mechanism behind Aap-mediated biofilm maturation, and also demonstrates a novel role for a secreted staphylococcal protease as a requirement for the development of a biofilm.

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“…“Biofilms grow virtually everywhere, in almost any environment where there is a combination of moisture, nutrients, and a surface.”20 Add in the inherent warmth of the lid margin and it makes an ideal surface for biofilm formation. When one considers that biofilms are found in deserts, on glaciers, and around deep-sea vents at the bottom of the ocean,21 it should come as no surprise that biofilms easily develop on the lid margin.…”

Section: Introductionmentioning

confidence: 99%

DEBS – a unification theory for dry eye and blepharitis

Rynerson¹,

Perry²

2016

OPTH

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For many years, blepharitis and dry eye disease have been thought to be two distinct diseases, and evaporative dry eye distinct from aqueous insufficiency. In this treatise, we propose a new way of looking at dry eye, both evaporative and insufficiency, as the natural sequelae of decades of chronic blepharitis. Dry eye is simply the late form and late manifestation of one disease, blepharitis. We suggest the use of a new term in describing this one chronic disease, namely dry eye blepharitis syndrome (DEBS). Bacteria colonize the lid margin within a structure known as a biofilm. The biofilm allows for population densities that initiate quorum-sensing gene activation. These newly activated gene products consist of inflammatory virulence factors, such as exotoxins, cytolytic toxins, and super-antigens, which are then present for the rest of the patient’s life. The biofilm never goes away; it only thickens with age, producing increasing quantities of bacterial virulence factors, and thus, increasing inflammation. These virulence factors are likely the culprits that first cause follicular inflammation, then meibomian gland dysfunction, aqueous insufficiency, and finally, after many decades, lid destruction. We suggest that there are four stages of DEBS which correlate with the clinical manifestations of folliculitis, meibomitis, lacrimalitis, and finally lid structure damage evidenced by entropion, ectropion, and floppy eyelid syndrome. When one fully understands the structure and location of the glands within the lid, it becomes easy to understand this staged disease process. The longer a gland can resist the relentless encroachment of the invading biofilm, the longer it can maintain normal function. The stages depend purely on anatomy and years of biofilm presence. Dry eye now becomes a very easy disease to understand. We feel that dry eye should be treated and prevented by early and routine biofilm removal through electromechanical lid margin debridement.

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Sub-inhibitory tigecycline concentrations induce extracellular matrix binding protein Embp dependent Staphylococcus epidermidis biofilm formation and immune evasion

Cited by 28 publications

References 58 publications

Microbial Biofilms and Chronic Wounds

Microbial Biofilms and Chronic Wounds

The metalloprotease SepA governs processing of accumulation‐associated protein and shapes intercellular adhesive surface properties in Staphylococcus epidermidis

DEBS – a unification theory for dry eye and blepharitis

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Sub-inhibitory tigecycline concentrations induce extracellular matrix binding protein Embp dependent Staphylococcus epidermidis biofilm formation and immune evasion

Cited by 28 publications

References 58 publications

Microbial Biofilms and Chronic Wounds

Microbial Biofilms and Chronic Wounds

The metalloprotease SepA governs processing of accumulation‐associated protein and shapes intercellular adhesive surface properties in Staphylococcus epidermidis

DEBS &ndash;&nbsp;a unification theory for dry eye and blepharitis

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DEBS – a unification theory for dry eye and blepharitis