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Cytochalasin B triggers a novel pertussis toxin sensitive pathway in TNF-alpha primed neutrophils
Johan Bylund, Sara Pellmé, Huamei Fu, Ulf-Henrik Mellqvist, Kristoffer Hellstrand, Anna Karlsson, Claes Dahlgren
BMC Cell Biology , 2004, DOI: 10.1186/1471-2121-5-21
Abstract: Tumor necrosis factor alpha (TNF-alpha) primes neutrophils for subsequent activation by cytochalasin B. Pretreatment with TNF-alpha induced mobilization of receptor-storing neutrophil organelles, suggesting that receptor up-regulation significantly contributes to the response, but the receptor mobilization was not sufficient for induction of the cytochalasin B sensitive state. The TNF-alpha primed state resembled that of the desensitized non-signaling state of agonist-occupied neutrophil formyl peptide receptors. The fact that the TNF-alpha primed, cytochalasin B-triggered activation process was pertussis toxin sensitive suggests that the activation process involves a GPCR. Based on desensitization experiments the unidentified receptor was found to be distinct from the C5a receptor as well as the formyl peptide receptor family members FPR and FPRL1. Based on the fact the occupied and desensitized receptors for interleukin-8 and platelet activating factor could not be reactivated by cytochalasin B, also these could be excluded as receptor candidates involved in the TNF-alpha primed state.The TNF-alpha-induced priming signals could possibly trigger a release of an endogenous GPCR-agonist, amplifying the response to the receptor-uncoupling effect of cytochalasin B. However, no such substance could be found, suggesting that TNF-alpha can transfer G-protein coupled receptors to a signaling state independently of agonist binding.Human neutrophil granulocytes constitute an important part of the innate immune defense against microbial infections, and the bactericidal activities performed by these cells rely on their interaction with chemoattractants, cytokines and other inflammatory mediators [1]. The chemoattractants, including C5a, platelet activating factor (PAF), interleukin-8 (IL8) and formylated peptides, bind to specific receptors [2,3], all of which belong to a family of transmembrane G-protein coupled receptors (GPCRs). Activation of these receptors leads to direct
Lectins Offer New Perspectives in the Development of Macrophage-Targeted Therapies for COPD/Emphysema
Violet R. Mukaro, Johan Bylund, Greg Hodge, Mark Holmes, Hubertus Jersmann, Paul N. Reynolds, Sandra Hodge
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056147
Abstract: We have previously shown that the defective ability of alveolar macrophages (AM) to phagocytose apoptotic cells (‘efferocytosis’) in chronic obstructive pulmonary disease/emphysema (COPD) could be therapeutically improved using the C-type lectin, mannose binding lectin (MBL), although the exact mechanisms underlying this effect are unknown. An S-type lectin, galectin-3, is also known to regulate macrophage phenotype and function, via interaction with its receptor CD98. We hypothesized that defective expression of galectin/CD98 would be associated with defective efferocytosis in COPD and that mechanisms would include effects on cytoskeletal remodeling and macrophage phenotype and glutathione (GSH) availability. Galectin-3 was measured by ELISA in BAL from controls, smokers and current/ex-smokers with COPD. CD98 was measured on AM using flow cytometry. We assessed the effects of galectin-3 on efferocytosis, CD98, GSH, actin polymerisation, rac activation, and the involvement of PI3K (using β-actin probing and wortmannin inhibition) in vitro using human AM and/or MH-S macrophage cell line. Significant decreases in BAL galectin-3 and AM CD98 were observed in BAL from both current- and ex-smoker COPD subjects vs controls. Galectin 3 increased efferocytosis via an increase in active GTP bound Rac1. This was confirmed with β-actin probing and the role of PI3K was confirmed using wortmannin inhibition. The increased efferocytosis was associated with increases in available glutathione and expression of CD98. We provide evidence for a role of airway lectins in the failed efferocytosis in COPD, supporting their further investigation as potential macrophage-targeted therapies.
Reactivation of Desensitized Formyl Peptide Receptors by Platelet Activating Factor: A Novel Receptor Cross Talk Mechanism Regulating Neutrophil Superoxide Anion Production
Huamei Forsman, Karin ?nnheim, Emil Andréasson, Karin Christenson, Anna Karlsson, Johan Bylund, Claes Dahlgren
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060169
Abstract: Neutrophils express different chemoattractant receptors of importance for guiding the cells from the blood stream to sites of inflammation. These receptors communicate with one another, a cross talk manifested as hierarchical, heterologous receptor desensitization. We describe a new receptor cross talk mechanism, by which desensitized formyl peptide receptors (FPRdes) can be reactivated. FPR desensitization is induced through binding of specific FPR agonists and is reached after a short period of active signaling. The mechanism that transfers the receptor to a non-signaling desensitized state is not known, and a signaling pathway has so far not been described, that transfers FPRdes back to an active signaling state. The reactivation signal was generated by PAF stimulation of its receptor (PAFR) and the cross talk was uni-directional. LatrunculinA, an inhibitor of actin polymerization, induced a similar reactivation of FPRdes as PAF while the phosphatase inhibitor CalyculinA inhibited reactivation, suggesting a role for the actin cytoskeleton in receptor desensitization and reactivation. The activated PAFR could, however, reactivate FPRdes also when the cytoskeleton was disrupted prior to activation. The receptor cross talk model presented prophesies that the contact on the inner leaflet of the plasma membrane that blocks signaling between the G-protein and the FPR is not a point of no return; the receptor cross-talk from the PAFRs to the FPRdes initiates an actin-independent signaling pathway that turns desensitized receptors back to a signaling state. This represents a novel mechanism for amplification of neutrophil production of reactive oxygen species.
Endogenous Acute Phase Serum Amyloid A Lacks Pro-Inflammatory Activity, Contrasting the Two Recombinant Variants That Activate Human Neutrophils through Different Receptors
Karin Christenson,Lena Bj?rkman,Sofie Ahlin,Maja Olsson,Kajsa Sj?holm,Anna Karlsson,Johan Bylund
Frontiers in Immunology , 2013, DOI: 10.3389/fimmu.2013.00092
Abstract: Most notable among the acute phase proteins is serum amyloid A (SAA), levels of which can increase 1000-fold during infections, aseptic inflammation, and/or trauma. Chronically elevated SAA levels are associated with a wide variety of pathological conditions, including obesity and rheumatic diseases. Using a recombinant hybrid of the two human SAA isoforms (SAA1 and 2) that does not exist in vivo, numerous in vitro studies have given rise to the notion that acute phase SAA is a pro-inflammatory molecule with cytokine-like properties. It is however unclear whether endogenous acute phase SAA per se mediates pro-inflammatory effects. We tested this in samples from patients with inflammatory arthritis and in a transgenic mouse model that expresses human SAA1. Endogenous human SAA did not drive production of pro-inflammatory IL-8/KC in either of these settings. Human neutrophils derived from arthritis patients displayed no signs of activation, despite being exposed to severely elevated SAA levels in circulation, and SAA-rich sera also failed to activate cells in vitro. In contrast, two recombinant SAA variants (the hybrid SAA and SAA1) both activated human neutrophils, inducing L-selectin shedding, production of reactive oxygen species, and production of IL-8. The hybrid SAA was approximately 100-fold more potent than recombinant SAA1. Recombinant hybrid SAA and SAA1 activated neutrophils through different receptors, with recombinant SAA1 being a ligand for formyl peptide receptor 2 (FPR2). We conclude that even though recombinant SAAs can be valuable tools for studying neutrophil activation, they do not reflect the nature of the endogenous protein.
The Human Neutrophil Subsets Defined by the Presence or Absence of OLFM4 Both Transmigrate into Tissue In Vivo and Give Rise to Distinct NETs In Vitro
Amanda Welin, Firoozeh Amirbeagi, Karin Christenson, Lena Bj?rkman, Halla Bj?rnsdottir, Huamei Forsman, Claes Dahlgren, Anna Karlsson, Johan Bylund
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0069575
Abstract: Neutrophil heterogeneity was described decades ago, but it could not be elucidated at the time whether the existence of different neutrophil subsets had any biological relevance. It has been corroborated in recent years that neutrophil subsets, defined by differential expression of various markers, are indeed present in human blood, calling for renewed attention to this question. The expression of the granule protein olfactomedin 4 (OLFM4) has been suggested to define two such neutrophil subsets. We confirm the simultaneous presence of one OLFM4-positive and one OLFM4-negative neutrophil subpopulation as well as the localization of the protein to specific granules. In vitro, these neutrophil subsets displayed equal tendency to undergo apoptosis and phagocytose bacteria. In addition, the subpopulations were recruited equally to inflammatory sites in vivo, and this was true both in an experimental model of acute inflammation and in naturally occurring pathological joint inflammation. In line with its subcellular localization, only limited OLFM4 release was seen upon in vivo transmigration, and release through conventional degranulation required strong secretagogues. However, extracellular release of OLFM4 could be achieved upon formation of neutrophil extracellular traps (NETs) where it was detected only in a subset of the NETs. Although we were unable to demonstrate any functional differences between the OLFM4-defined subsets, our data show that different neutrophil subsets are present in inflamed tissue in vivo. Furthermore, we demonstrate NETs characterized by different markers for the first time, and our results open up for functions of OLFM4 itself in the extracellular space through exposure in NETs.
Mice Chronically Fed High-Fat Diet Have Increased Mortality and Disturbed Immune Response in Sepsis
Louise Strandberg,Margareta Verdrengh,Maria Enge,Niklas Andersson,Sylvie Amu,Karin ?nnheim,Anna Benrick,Mikael Brisslert,Johan Bylund,Maria Bokarewa,Staffan Nilsson,John-Olov Jansson
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0007605
Abstract: Sepsis is a potentially deadly disease that often is caused by gram-positive bacteria, in particular Staphylococcus aureus (S. aureus). As there are few effective therapies for sepsis, increased basic knowledge about factors predisposing is needed.
On the existence of doubling measures with certain regularity properties
Per Bylund,Jaume Gudayol
Mathematics , 1998,
Abstract: Given a compact pseudo-metric space, we associate to it upper and lower dimensions, depending only on the metric. Then we construct a doubling metric for which the measure of a dillated ball is closely related to these dimensions.
Carter's constant revealed
Kjell Rosquist,Tomas Bylund,Lars Samuelsson
Physics , 2007, DOI: 10.1142/S0218271809014546
Abstract: A new formulation of Carter's constant for geodesic motion in Kerr black holes is given. It is shown that Carter's constant corresponds to the total angular momentum plus a precisely defined part which is quadratic in the linear momenta. The characterization is exact in the weak field limit obtained by letting the gravitational constant go to zero. It is suggested that the new form can be useful in current studies of the dynamics of extreme mass ratio inspiral (EMRI) systems emitting gravitational radiation.
The Ubiquitous Interactor - Device Independent Access to Mobile Services
Stina Nylander,Markus Bylund,Annika Waern
Computer Science , 2003,
Abstract: The Ubiquitous Interactor (UBI) addresses the problems of design and development that arise around services that need to be accessed from many different devices. In UBI, the same service can present itself with different user interfaces on different devices. This is done by separating interaction between users and services from presentation. The interaction is kept the same for all devices, and different presentation information is provided for different devices. This way, tailored user interfaces for many different devices can be created without multiplying development and maintenance work. In this paper we describe the system design of UBI, the system implementation, and two services implemented for the system: a calendar service and a stockbroker service.
Properties of Lorenz Curves for Transformed Income Distributions  [PDF]
Johan Fellman
Theoretical Economics Letters (TEL) , 2012, DOI: 10.4236/tel.2012.25091
Abstract: Redistributions of income can be considered as variable transformations of the initial income variable. The transformation is usually assumed to be positive, monotone-increasing and continuous, but discontinuous transformations have also been discussed recently. If the transformation is a tax or a transfer policy, the transformed variable is either the post-tax or the post-transfer income. A central problem has been the Lorenz dominance between the initial and the transformed income. This study considers analyses of other properties of the transformed Lorenz curves, especially its limits. We take in account mainly two cases (a) the transformed variable Lorenz dominates the initial one and (b) the initial Lorenz dominates the transformed one. For applications, the first case is more important than the second. The limits obtained are not accurate for a specific transformation, but do hold generally for all distributions and a broad class of transformations so that, if one pursues general conditions the inequalities obtained cannot be improved.
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