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      Capsular contracture around silicone miniimplants following bacterial contamination: an in vivo comparative experimental study between textured and polyurethane implants

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          Abstract

          <p class="first" id="d5932555e125">Capsular contracture remains a problem following breast implant surgery. Although impact of biofilm and implant surface on capsule formation has been demonstrated, interaction of microorganisms with different surface types has not been clarified yet. We aimed to compare the ability of biofilm formation of implants with different surfaces, under standard conditions and to demonstrate its impact on capsular contracture. </p>

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          Role of Human Macrophage Polarization in Inflammation during Infectious Diseases

          Chiraz Atri, Fatma Z. Guerfali, Dhafer Laouini (2018)
          Experimental models have often been at the origin of immunological paradigms such as the M1/M2 dichotomy following macrophage polarization. However, this clear dichotomy in animal models is not as obvious in humans, and the separating line between M1-like and M2-like macrophages is rather represented by a continuum, where boundaries are still unclear. Indeed, human infectious diseases, are characterized by either a back and forth or often a mixed profile between the pro-inflammatory microenvironment (dominated by interleukin (IL)-1β, IL-6, IL-12, IL-23 and Tumor Necrosis Factor (TNF)-α cytokines) and tissue injury driven by classically activated macrophages (M1-like) and wound healing driven by alternatively activated macrophages (M2-like) in an anti-inflammatory environment (dominated by IL-10, Transforming growth factor (TGF)-β, chemokine ligand (CCL)1, CCL2, CCL17, CCL18, and CCL22). This review brews the complexity of the situation during infectious diseases by stressing on this continuum between M1-like and M2-like extremes. We first discuss the basic biology of macrophage polarization, function, and role in the inflammatory process and its resolution. Secondly, we discuss the relevance of the macrophage polarization continuum during infectious and neglected diseases, and the possibility to interfere with such activation states as a promising therapeutic strategy in the treatment of such diseases.
          Article 0 comments Cited 482 times – based on 0 reviews     Review now
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            Tolerance to the antimicrobial peptide colistin in Pseudomonas aeruginosa biofilms is linked to metabolically active cells, and depends on the pmr and mexAB-oprM genes.

            Tim Tolker-Nielsen, Helle Krogh Johansen, Sünje J Pamp … (2008)
            Bacteria living as biofilm are frequently reported to exhibit inherent tolerance to antimicrobial compounds, and might therefore contribute to the persistence of infections. Antimicrobial peptides are attracting increasing interest as new potential antimicrobial therapeutics; however, little is known about potential mechanisms, which might contribute to resistance or tolerance development towards these compounds in biofilms. Here we provide evidence that a spatially distinct subpopulation of metabolically active cells in Pseudomonas aeruginosa biofilms is able to develop tolerance to the antimicrobial peptide colistin. On the contrary, biofilm cells exhibiting low metabolic activity were killed by colistin. We demonstrate that the subpopulation of metabolically active cells is able to adapt to colistin by inducing a specific adaptation mechanism mediated by the pmr operon, as well as an unspecific adaptation mechanism mediated by the mexAB-oprM genes. Mutants defective in either pmr-mediated lipopolysaccharide modification or in mexAB-oprM-mediated antimicrobial efflux were not able to develop a tolerant subpopulation in biofilms. In contrast to the observed pattern of colistin-mediated killing in biofilms, conventional antimicrobial compounds such as ciprofloxacin and tetracycline were found to specifically kill the subpopulation of metabolically active biofilm cells, whereas the subpopulation exhibiting low metabolic activity survived the treatment. Consequently, targeting the two physiologically distinct subpopulations by combined antimicrobial treatment with either ciprofloxacin and colistin or tetracycline and colistin almost completely eradicated all biofilm cells.
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              Biofilm formation and dispersal and the transmission of human pathogens.

              Paul Stoodley, Luanne Hall-Stoodley (2004)
              Several pathogenic bacterial species that are found in the environment can form complex multicellular structures on surfaces known as biofilms. Pseudomonas aeruginosa, Vibrio cholerae and certain species of nontuberculous mycobacteria are examples of human pathogens that form biofilms in natural aquatic environments. We suggest that the dynamics of biofilm formation facilitates the transmission of pathogens by providing a stable protective environment and acting as a nidus for the dissemination of large numbers of microorganisms; both as detached biofilm clumps and by the fluid-driven dispersal of biofilm clusters along surfaces. We also suggest that emerging evidence indicates that biofilm formation conveys a selective advantage to certain pathogens by increasing their ability to persist under diverse environmental conditions.
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                Author and article information

                Contributors
                Esra Özkoçer: (View ORCID Profile)
                Journal
                Title: Journal of Plastic, Reconstructive & Aesthetic Surgery
                Abbreviated Title: Journal of Plastic, Reconstructive & Aesthetic Surgery
                Publisher: Elsevier BV
                ISSN (Print): 17486815
                Publication date Created: September 2020
                Publication date (Print): September 2020
                Volume: 73
                Issue: 9
                Pages: 1747-1757
                Article
                DOI: 10.1016/j.bjps.2020.02.049
                PubMed ID: 32278659
                SO-VID: 28a34b90-f020-432f-a2b4-4d416a50dbe5
                Copyright © © 2020
                License:

                https://www.elsevier.com/tdm/userlicense/1.0/

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