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1.
  • Almkvist, Jenny, 1971, et al. (creator_code:aut_t)
  • Galectins as inflammatory mediators.
  • 2004
  • record:In_t: Glycoconjugate journal. - 0282-0080. ; 19:7-9, s. 575-81
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Over the last decade a vast amount of reports have shown that galectin-1 and galectin-3 are important mediators of inflammation. In this review we describe how the galectins may be involved in several parts of the inflammatory process, including the recruitment of neutrophils into an infected tissue and the recognition and killing of bacteria by activation of the tissue destructive phagocytic respiratory burst. During bacterial infection or aseptic inflammatory processes, galectins are produced and released by e.g. infected epithelium, activated tissue-resident macrophages and endothelial cells. These extracellular galectins may facilitate binding of neutrophils to the endothelium by cross-linking carbohydrates on the respective cells. Further the galectins improve binding of the neutrophil to the extracellular matrix proteins laminin and fibronectin, and are potential chemotactic factors, inducing migration through the extracellular matrix towards the inflammatory focus. When the cells encounter bacteria, galectin-3 could function as an opsonin, cross-linking bacterial lipopolysaccharide or other carbohydrate-containing surface structures to phagocyte surface glycoconjugates. Both galectin-1 and galectin-3 have the capacity to induce a respiratory burst in neutrophils, provided that the cells have been primed by degranulation and receptor upregulation. The reactive oxygen species produced may be destructive to the invading micro-organisms as well as to the surrounding host tissue, pointing out the possible role of galectins, not only in defence toward infection, but also in inflammatory-induced tissue destruction.
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3.
  • Björstad, Åse, 1976, et al. (creator_code:aut_t)
  • Antimicrobial host defence peptides of human neutrophils – roles in innate immunity
  • 2008
  • record:In_t: Anti-Infective Agents in Medicinal Chemistry. - : Bentham Science Publishers Ltd.. - 1871-5214. ; 7:3, s. 155-168
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • The innate immune system is an old defence mechanism that in primitive organisms consists mainly of humoral components like antimicrobial peptides. Many of these peptides share features such as size, cationicity, amphipathicity and kill microbes primarily by lysing the cell membrane. In more evolved organisms, humoral factors are supplemented by cellular components such as professional phagocytes, but the antimicrobial peptides are still important for host defence. Neutrophils are professional phagocytes that in humans contain two different classes of classical antimicrobial peptides belonging to the cathelicidin family and the α-defensin family, respectively. In addition to these two main groups of poly-peptides, neutrophils are also rich in antimicrobial proteins. It is becoming increasingly clear that the antimicrobial peptides of neutrophils not only contribute to phagosomal killing, but also function as regulators of immunity; therefore the alternative name host defence peptides is more appropriate. The question whether antimicrobial host defence peptides are primarily immunomodulatory or antimicrobial in vivo has not been conclusively determined. At some locations in the body, e.g. in a phagosome, their effect is likely directly antimicrobial, whereas their immunomodulatory functions are probably more important at other sites. This review will provide a background to the field of antimicrobial peptides including their common features, mechanisms of killing and availability in nature. It will focus on the antimicrobial peptides present in human neutrophils and special emphasis will be given to the functional dualism displayed by many peptides giving them the ability to modulate the immune response in addition to being directly antimicrobial
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  • Bylund, Johan, 1975, et al. (creator_code:aut_t)
  • Intracellular generation of superoxide by the phagocyte NADPH oxidase: How, where, and what for?
  • 2010
  • record:In_t: Free radical biology & medicine. - : Elsevier BV. - 1873-4596 .- 0891-5849.
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Professional phagocytes increase their consumption of molecular oxygen during the phagocytosis of microbes or when encountering a variety of nonparticulate stimuli. In these circumstances, oxygen is reduced by the phagocyte NADPH oxidase, and reactive oxygen species (ROS), which are important for the microbicidal activity of the cells, are generated. The structure and function of the NADPH oxidase have been resolved in part by studying cells from patients with chronic granulomatous disease (CGD), a condition characterized by the inability of phagocytes to assemble a functional NADPH oxidase and thus to produce ROS. As a result, patients with CGD have a predisposition to infections as well as a variety of inflammatory symptoms. A long-standing paradigm has been that NADPH oxidase assembly occurs exclusively in the plasma membrane or invaginations thereof (phagosomes). A growing body of evidence points to the possibility that phagocytes are capable of NADPH oxidase assembly in nonphagosomal intracellular membranes, resulting in ROS generation within intracellular organelles also in the absence of phagocytosis. The exact nature of these ROS-producing organelles is yet to be determined, but granules are prime suspects. Recent clinical findings indicate that the generation of intracellular ROS by NADPH oxidase activation is important for limiting inflammatory reactions and that intracellular and extracellular ROS production are regulated differently. Here we discuss the accumulating knowledge of intracellular ROS production in phagocytes and speculate on the precise role of these oxidants in regulating the inflammatory process.
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6.
  • Bylund, Johan, 1975, et al. (creator_code:aut_t)
  • Measurement of respiratory burst products, released or retained, during activation of professional phagocytes.
  • 2014
  • record:In_t: Methods in molecular biology (Clifton, N.J.). - Totowa, NJ : Humana Press. - 1940-6029. ; 1124, s. 321-38
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • Activation of professional phagocytes, potent microbial killers of our innate immune system, is associated with an increase in cellular consumption of molecular oxygen (O2). The consumed O2 is utilized by an NADPH-oxidase to generate highly reactive oxygen species (ROS) by a one electron reduction, initially generating superoxide anion (O2 (-)) that then dismutates to hydrogen peroxide (H2O2). The ROS are strongly bactericidal molecules but may also cause tissue destruction, and are capable of driving immune competent cells of both the innate and the adaptive immune systems into apoptosis. The development of basic techniques to measure/quantify ROS generation by phagocytes during activation of the respiratory burst is of great importance, and a large number of methods have been used for this purpose. A selection of methods, including chemiluminescence amplified by luminol or isoluminol, the absorbance change following reduction of cytochrome c, and the fluorescence increase upon oxidation of PHPA, are described in detail in this chapter with special emphasis on how to distinguish between ROS that are released extracellularly, and those that are retained within intracellular organelles. These techniques can be valuable tools in research spanning from basic phagocyte biology to more clinically oriented research on innate immune mechanisms and inflammation.
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7.
  • Christenson, Karin, et al. (creator_code:aut_t)
  • Collection of in vivo transmigrated neutrophils from human skin.
  • 2014
  • record:In_t: Methods in molecular biology (Clifton, N.J.). - Totowa, NJ : Humana Press. - 1940-6029. ; 1124, s. 39-52
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • A wealth of knowledge on the life and death of human neutrophils has been obtained by the in vitro study of isolated cells derived from peripheral blood. However, neutrophils are of main importance, physiologically as well as pathologically, after they have left circulation and transmigrated to extravascular tissues. The journey from blood to tissue is complex and eventful, and tissue neutrophils are in many aspects distinct from the cells left in circulation. Here we describe how to obtain human tissue neutrophils in a controlled experimental setting from aseptic skin lesions created by the application of negative pressure. One protocol enables the direct analysis of the blister content, infiltrating leukocytes as well as exudate fluid, and is a simple method to follow multiple parameters of aseptic inflammation in vivo. Also described is the skin chamber technique, a method based on denuded skin blisters which are subsequently covered by collection chambers filled with autologous serum. Although slightly more artificial as compared to analysis of the blister content directly, the cellular yield of this skin chamber method is sufficient to perform a large number of functional analyses of in vivo transmigrated cells.
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8.
  • Dahlgren, Claes, 1949, et al. (creator_code:aut_t)
  • Respiratory burst in human neutrophils.
  • 1999
  • record:In_t: Journal of immunological methods. - 0022-1759. ; 232:1-2, s. 3-14
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • During phagocytosis of microbial intruders, professional phagocytes of our innate immune system increase their oxygen consumption through the activity of an NADPH-oxidase that generates superoxide anion (O(2)(-)) and hydrogen peroxide (H(2)O(2)). These oxygen metabolites give rise to yet other reactive oxygen species that are strongly anti-microbial but which may also cause damage by destructing surrounding tissue and inducing apoptosis in other immune reactive cells. The development of methodology to measure the generation/release of phagocyte respiratory burst products is thus of great importance, and a number of different techniques are currently in use for this purpose. Three of the techniques that we have used, (luminol/isoluminol amplified chemiluminescence, cytochrome C reduction, and PHPA oxidation technique) are described in more detail in this review. We hope to convince the readers that these techniques are valuable tools in basic as well as more clinically oriented research dealing with phagocyte function. The basic principles for luminol/isoluminol-amplified chemiluminescence is used as the starting point for discussing methodological problems related to measurements of oxygen metabolites generated by professional phagocytes.
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