Polarization of Macrophages, Cellular Adhesion, and Spreading on Bacterially Contaminated Gold Nanoparticle-Coatings in Vitro
Yafei LuanHenny C. van der MeiMelissa DijkGésinda I. Geertsema-DoornbuschJelly Atema‐SmitYijin RenHong ChenHenk J. Busscher
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Abstract:
Biomaterial-associated infections often arise from contaminating bacteria adhering to an implant surface that are introduced during surgical implantation and not effectively eradicated by antibiotic treatment. Whether or not infection develops from contaminating bacteria depends on an interplay between bacteria contaminating the biomaterial surface and tissue cells trying to integrate the surface with the aid of immune cells. The biomaterial surface plays a crucial role in defining the outcome of this race for the surface. Tissue integration is considered the best protection of a biomaterial implant against infectious bacteria. This paper aims to determine whether and how macrophages aid osteoblasts and human mesenchymal stem cells to adhere and spread over gold nanoparticle (GNP)-coatings with different hydrophilicity and roughness in the absence or presence of contaminating, adhering bacteria. All GNP-coatings had identical chemical surface composition, and water contact angles decreased with increasing roughness. Upon increasing the roughness of the GNP-coatings, the presence of contaminating Staphylococcus epidermidis in biculture with cells gradually decreased surface coverage by adhering and spreading cells, as in the absence of staphylococci. More virulent Staphylococcus aureus fully impeded cellular adhesion and spreading on smooth gold- or GNP-coatings, while Escherichia coli allowed minor cellular interaction. Murine macrophages in monoculture tended toward their pro-inflammatory “fighting” M1-phenotype on all coatings to combat the biomaterial, but in bicultures with contaminating, adhering bacteria, macrophages demonstrated Ym1 expression, indicative of polarization toward their anti-inflammatory “fix-and-repair” M2-phenotype. Damage repair of cells by macrophages improved cellular interactions on intermediately hydrophilic/rough (water contact angle 30 deg/surface roughness 118 nm) GNP-coatings in the presence of contaminating, adhering Gram-positive staphylococci but provided little aid in the presence of Gram-negative E. coli. Thus, the merits on GNP-coatings to influence the race for the surface and prevent biomaterial-associated infection critically depend on their hydrophilicity/roughness and the bacterial strain involved in contaminating the biomaterial surface.Keywords:
Biomaterial
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Macrophage influences peripheral nerve regeneration. According to the classical M1/M2 paradigm, the M1 macrophage is an inhibitor of regeneration, while the M2 macrophage is a promoter. However, several studies have shown that M1 macrophages are indispensable for peripheral nerve repair and facilitate many critical processes in axonal regeneration. In this review, we summarized the information on macrophage polarization and focused on the activities of M1 macrophages in regeneration. We also provided some examples where the macrophage phenotypes were regulated to help regeneration. We argued that the coordination of both macrophage phenotypes might be effective in peripheral nerve repair, and a more comprehensive view of macrophages might contribute to macrophage-based immunomodulatory therapies.
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Efforts in experimental therapeutics of atherosclerosis are mostly focused on identifying candidate targets that can be exploited in developing new strategies to reduce plaque progression, induce its regression and/or improve stability of advanced lesions. Plaque macrophages are central players in all these processes, and consequently a significant amount of research is devoted to understanding mechanisms that regulate, for instance, macrophage apoptosis, necrosis or migration. Macrophage diversity is a key feature of the macrophage population in the plaque and can impact many aspects of lesion development. Thus, searching for molecular entities that contribute to atherorelevant functions of a specific macrophage type but not others may lead to identification of targets that can be exploited in phenotype selective modulation of the lesional macrophage. This however, remains an unmet goal. In recent years several studies have revealed critical functions of micro-RNAs (miRs) in mechanisms of macrophage polarization, and a number of miRs have emerged as being specific of distinctive macrophage subsets. Not only can these miRs represent the first step towards recognition of phenotype specific targets, but they may also pave the way to reveal novel atherorelevant pathways within macrophage subsets. This article discusses some of these recent findings, speculates on their potential relevance to atherosclerosis and elaborates on the prospective use of miRs to affect the function of plaque macrophages in a phenotype selective manner.
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Macrophages have long been known for their phagocytic capabilities and immune defence; however, their role in healing is being increasingly recognized in recent years due to their ability to polarize into pro-inflammatory and anti-inflammatory phenotypes. Historically, biomaterials were designed to be inert to minimize the host response. More recently, the emergence of tissue engineering and regenerative medicine has led to the design of biomaterials that interact with the host through tailored mechanical, chemical and temporal characteristics. Due to such advances in biomaterial functionality and an improved understanding of macrophage responses to implanted materials, it is now possible to identify biomaterial design characteristics that dictate the host response and contribute to successful tissue integration. Herein, we begin by briefly reviewing macrophage cell origin and the key cytokine/chemokine markers of macrophage polarization and then describe which responses are favorable for both replacement and regenerative biomaterials. The body of the review focuses on macrophage polarization in response to inherent cues directly provided by biomaterials and the consequent cues that result from events related to biomaterial implantation. To conclude, a section on potential design principles for both replacement and regenerative biomaterials is presented. An in depth understanding of biomaterial cues to selectively polarize macrophages may prove beneficial in the design of a new generation of ‘immuno-informed’ biomaterials that can positively interact with the immune system to dictate a favorable macrophage response following implantation.
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Obesity and type 2 diabetes are now recognized as chronic pro-inflammatory diseases. In the last decade, the role of the macrophage in particular has become increasingly implicated in their pathogenesis. Abundant literature now establishes that monocytes get recruited to peripheral tissues (ie pancreas, liver and adipose tissue) to become resident macrophages and contribute to local inflammation, development of insulin resistance or even pancreatic dysfunction. Furthermore, an accumulation of evidence has established an important role for macrophage polarisation in the development of metabolic diseases. The general view in obesity is that there is an imbalance in the ratio of M1/M2 macrophages, with M1 “pro-inflammatory” macrophages being enhanced compared with M2 “anti-inflammatory” macrophages being down-regulated, leading to chronic inflammation and the propagation of metabolic dysfunction. However, there is emerging evidence revealing a more complex scenario with the spectrum of macrophage states exceeding well beyond the M1/M2 binary classification and confused further by human and animal models exhibiting different macrophage profiles. In this review we will discuss the recent findings regarding macrophage polarization in obesity and type 2 diabetes.
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Age-related macular degeneration (AMD) is one of the leading causes to blindness worldwide in elderly population.Innate immune system elements, such as macrophages and cytokines, play an important role in AMD pathology and pathogenesis.In AMD, macrophages can be functionally polarized into M1 (classically activated) and M2 (alternatively activated), as well as regulatory cells, in response to systems biology approaches.Imbalances in the M1 and M2 populations together with activation of retinal microglia are observed and potentially contribute to tissue degeneration.In this review, the phenomenon of macrophage polarization in AMD study was summarized, and the relationship between macrophage polarization and dry AMD, wet AMD, AMD related risk factors were discussed.
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Age-related macular degeneration; Macrophage polarization; M1 macrophage; M2 macrophage
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