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Phagocyte Activation (phagocyte + activation)
Selected AbstractsPhagocyte activation in preterm infants following premature rupture of the membranes or chorioamnionitisACTA PAEDIATRICA, Issue 10 2000I Nupponen Phagocyte activation was studied in 48 preterm infants, gestational age 27.3 ± 0.3 wk, birthweight 968 ± 40 g, during the first postnatal week. Human neutrophil lipocalin as a marker of neutrophil activation was measured in plasma and tracheal aspirate fractions; and lysozyme, as a marker of monocyte and macrophage activation, in plasma. The concentration of plasma human neutrophil lipocalin was 69 (46,126) ,g/l (median and quartiles), tracheal aspirate fraction fluid 213 (71,433) (,g/l and plasma lysozyme 1337 (923,1764) ,g/l. Infants born to mothers with premature rupture of the membranes or clinical chorioamnionitis (group A, n 20) had significantly higher plasma [73 (58,151) vs 53 (38,108) ,g/l; p 0.027], and tracheal aspirate fraction human neutrophil lipocalin [319 (129,540) vs 190 (57,324) ,g/l; p= 0.019], and plasma lysozyme [1739 (1356,2021) vs 1140 (739,1557) ,g/l; p 0.0001] than did infants whose mothers had intact membranes and who had no suspicion of infection (Group B, n 28). In infants born to mothers receiving corticosteroids ante partum, correlations existed between time from treatment to delivery and plasma (r 0.322, p 0.0256) and tracheal aspirate fraction human neutrophil lipocalin (r= 0.314, p 0.0096). Infants born to mothers with at risk of infection are exposed to the potentially harmful effects of activated neutrophils. Premature rupture of the membranes, even without signs of clinical infection of the mother or the fetus, is associated with phagocyte activation that may begin already in utero. Corticosteroid treatment of the mother may cause transient inhibition of neutrophil activation in the newborn. [source] Activation and deactivation of periventricular white matter phagocytes during postnatal mouse developmentGLIA, Issue 1 2010Mariya Hristova Abstract Brain microglia are related to peripheral macrophages but undergo a highly specific process of regional maturation and differentiation inside the brain. Here, we examined this deactivation and morphological differentiation in cerebral cortex and periventricular subcortical white matter, the main "fountain of microglia" site, during postnatal mouse development, 0,28 days after birth (P0,P28). Only macrophages in subcortical white matter but not cortical microglia exhibited strong expression of typical activation markers alpha5, alpha6, alphaM, alphaX, and beta2 integrin subunits and B7.2 at any postnatal time point studied. White matter phagocyte activation was maximal at P0, decreased linearly over P3 and P7 and disappeared at P10. P7 white matter phagocytes also expressed high levels of IGF1 and MCSF, but not TNFalpha mRNA; this expression disappeared at P14. This process of deactivation followed the presence of ingested phagocytic material but correlated only moderately with ramification, and not with the extent of TUNEL+ death in neighboring cells, their ingestion or microglial proliferation. Intravenous fluosphere labeling revealed postnatal recruitment and transformation of circulating leukocytes into meningeal and perivascular macrophages as well as into ramified cortical microglia, but bypassing the white matter areas. In conclusion, this study describes strong and selective activation of postnatally resident phagocytes in the P0,P7 subcortical white matter, roughly equivalent to mid 3rd trimester human fetal development. This presence of highly active and IGF1- and MCSF-expressing phagocytes in the neighborhood of vulnerable white matter could play an important role in the genesis of or protection against axonal damage in the fetus and premature neonate. © 2009 Wiley-Liss, Inc. [source] Amyloid precursor protein-processing products affect mononuclear phagocyte activation: pathways for sAPP- and A,-mediated neurotoxicityJOURNAL OF NEUROCHEMISTRY, Issue 4 2003Tsuneya Ikezu Abstract Increasing evidence strongly supports the role of glial immunity in the pathogenesis of Alzheimer's disease (AD). To investigate such events we have developed cell systems mimicking the interactions between ,-amyloid precursor protein (APP)-expressing neurons and brain mononuclear phagocytes (MP; macrophages and microglia). MP were co-cultured with neuronal cells expressing wild type APP or familial AD-linked APP mutants. The latter was derived from recombinant adenoviral constructs. Neuronal APP processing products induced MP activation, reactive oxygen species, and neurotoxic activities. These occurred without the addition of pro-inflammatory cytokines and were reversed by depletion of amyloid ,-peptide (A,) and secreted APP (sAPP). Neurotoxic activities were diminished by superoxide dismutase mimetics and NMDA receptor inhibitors. Microglial glutamate secretion was suppressed by the cystine-glutamate antiporter inhibitor and its levels paralleled the depletion of sAPP and A, from conditioned media prepared from APP-expressing neurons. The excitotoxins from activated MP were potent enough to evoke recombinant NMDA receptor-mediated inward currents expressed in vitro in the Xenopus oocytes. These results demonstrate that neuronal APP-processing products can induce oxidative neurotoxicity through microglial activation. [source] | ||||||||||