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Sökning: LAR1:gu > Forskningsöversikt > Bylund Johan 1975

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  • Björstad, Åse, 1976, et al. (författare)
  • Antimicrobial host defence peptides of human neutrophils – roles in innate immunity
  • 2008
  • Ingår i: Anti-Infective Agents in Medicinal Chemistry. - : Bentham Science Publishers Ltd.. - 1871-5214. ; 7:3, s. 155-168
  • Forskningsöversikt (refereegranskat)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. (författare)
  • Intracellular generation of superoxide by the phagocyte NADPH oxidase: How, where, and what for?
  • 2010
  • Ingår i: Free radical biology & medicine. - : Elsevier BV. - 1873-4596 .- 0891-5849.
  • Forskningsöversikt (refereegranskat)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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  • Bylund, Johan, 1975, et al. (författare)
  • Measurement of respiratory burst products, released or retained, during activation of professional phagocytes.
  • 2014
  • Ingår i: Methods in molecular biology (Clifton, N.J.). - Totowa, NJ : Humana Press. - 1940-6029. ; 1124, s. 321-38
  • Forskningsöversikt (refereegranskat)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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  • Bylund, Johan, 1975, et al. (författare)
  • Turning Chemoattractant Receptors On and Off with Conventional Ligands and Allosteric Modulators: Recent advances in formyl peptide receptor signaling and regulation
  • 2014
  • Ingår i: Inflammation and cell signaling. - : Smart Science and Technology, LLC. - 2330-7803 .- 2330-7803 .- 2330-779X. ; 1:1
  • Forskningsöversikt (refereegranskat)abstract
    • Recruitment and activation of neutrophils at sites of infection/inflammation relies largely on the surface expression of G-protein coupled receptors (GPCRs) that recognize chemoattractants. One of these receptors, FPR1, for which formylated peptides generated by bacteria and mitochondria are high affinity agonists, was among the first human neutrophil GPCR to being cloned. This receptor shares large sequence homologies with FPR2, another member of the FPR-family expressed in human neutrophils and having a distinct ligand binding profile. The two FPRs transduce very similar neutrophil responses but possess somewhat different regulatory profiles. The FPRs have served as excellent model receptors in studies attempting to understand not only GPCR related regulation in general, but also receptor signaling in relation to innate immune reactivity and inflammation. Recent research has identified not only a large number of conventional ligands (agonist/antagonists) that regulate FPR activities by binding to surface exposed parts of the receptors, but also a number of membrane penetrating molecules that allosterically modulate receptor function after passing the membrane and interacting with the receptor on the cytosolic side. After activation, FPR signaling is rapidly terminated and the receptors become desensitized, a dormant state that can be achieved by multiple mechanisms. A coupling of the activated receptors to the actin cytoskeleton in a process that physically separates the receptors from the signaling G-protein is one such mechanism. Traditionally, the desensitized state has been viewed as a point of no return, but recent findings challenge this view and demonstrate that desensitized FPRs may in fact be reactivated to resume active signaling. The FPRs have also the capacity to communicate with other receptors in a hierarchical manner and this receptor cross-talk can both dampen and amplify neutrophil responses. In this review, we summarize some recent advances of our understanding how the FPRs can be turned on and off and discuss some future challenges, including mechanisms of allosteric modulation, receptor cross-talk, and FPR reactivation.
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  • Christenson, Karin, et al. (författare)
  • Analyzing cell death events in cultured leukocytes.
  • 2012
  • Ingår i: Methods in molecular biology (Clifton, N.J.). - Totowa, NJ : Humana Press. - 1940-6029. ; 844, s. 65-86
  • Forskningsöversikt (refereegranskat)abstract
    • Cell death is of utmost importance in immunity, in part as a way to control the development and activity of leukocytes, but also as a strategy employed by leukocytes to rid the body of unwanted cells. Apoptosis is the classic type of programmed cell death involving an ordered sequence of cellular events, resulting in morphological changes that include cleavage/fragmentation of DNA, condensation of nuclei, cell shrinkage, and alterations of the plasma membrane. The apoptotic cell is a nonfunctional, but structurally intact, entity with preserved membrane integrity that is engulfed by surrounding cells (a process known as clearance) in an immunologically silent manner. In contrast, necrotic cells, i.e., nonfunctional cells that have lost membrane integrity, are freely permeable and leak intracellular constituents that may shift immunological homeostasis. Thus, membrane integrity of dead leukocytes is very important from an immunological point of view. For the analysis of leukocyte cell death, a wide variety of assays are available to monitor different events along the cell death pathway; a combination of different methods is advantageous in order to gain a more complete understanding of this dynamic process. In this chapter, we describe several in vitro methods for evaluating leukocyte cell death, mainly focusing on apoptosis in human neutrophils and lymphocytes. Special emphasis is given to assessment of membrane integrity of the cultured cells. Furthermore, a protocol for monitoring clearance of apoptotic neutrophils by monocyte-derived macrophages is provided.
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  • Christenson, Karin, et al. (författare)
  • Collection of in vivo transmigrated neutrophils from human skin.
  • 2014
  • Ingår i: Methods in molecular biology (Clifton, N.J.). - Totowa, NJ : Humana Press. - 1940-6029. ; 1124, s. 39-52
  • Forskningsöversikt (refereegranskat)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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