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Murine Peritoneal Macrophages (murine + peritoneal_macrophage)
Selected AbstractsAdrenaline inhibits macrophage nitric oxide production through ,1 and ,2 adrenergic receptorsIMMUNOLOGY, Issue 3 2000L. B. Sigola Summary This study was conducted to investigate the role of the acute stress hormone adrenaline on macrophage nitric oxide (NO) production. Murine peritoneal macrophages were stimulated in vitro with lipopolysaccharide (LPS) in the absence or presence of adrenaline. Adrenaline inhibited the LPS-induced nitrite response in a dose-dependent manner. The suppressive effect of adrenaline on NO production was mediated via ,1 and ,2 adrenergic receptors since isoprenaline (a non-selective ,1 and ,2 agonist), dobutamine and salbutamol (selective ,1 and ,2 agonists, respectively) had similar effects on the NO response. In addition, the inhibitory effect of adrenaline on NO was abrogated by both propranolol (a non-specific , blocker) and atenolol (a specific ,1 inhibitor). In contrast to , receptor activation, the , adrenergic agonist phenylephrine had no effect on the LPS NO response, and furthermore, phentolamine (an , receptor antagonist) did not ameliorate adrenaline's inhibitory action. [source] Inhibition of interferon-,-induced nitric oxide production in endotoxin-activated macrophages by cytolethal distending toxinMOLECULAR ORAL MICROBIOLOGY, Issue 5 2008K. P. S. Fernandes Introduction:, Cytolethal distending toxin (CDT) is a DNA-targeting agent produced by certain pathogenic gram-negative bacteria such as the periodontopathogenic organism Aggregatibacter actinomycetemcomitans. CDT targets lymphocytes and other cells causing cell cycle arrest and apoptosis, impairing the host immune response and contributing to the persistence of infections caused by this microorganism. In this study we explored the effects of CDT on the innate immune response, by investigating how it affects production of nitric oxide (NO) by macrophages. Methods:, Murine peritoneal macrophages were stimulated with Escherichia coli sonicates and NO production was measured in the presence or not of active CDT. Results:, We observed that CDT promptly and significantly inhibited NO production by inducible nitric oxide synthase (iNOS) in a dose-dependent manner. This inhibition is directed towards interferon-,-dependent pathways and is not mediated by either interleukin-4 or interleukin-10. Conclusion:, This mechanism may constitute an important aspect of the immunosuppression mediated by CDT and may have potential clinical implications in A. actinomycetemcomitans infections. [source] NTPDase1 governs P2X7 -dependent functions in murine macrophagesEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2010Sébastien A. Lévesque Abstract P2X7 receptor is an adenosine triphosphate (ATP)-gated ion channel within the multiprotein inflammasome complex. Until now, little is known about regulation of P2X7 effector functions in macrophages. In this study, we show that nucleoside triphosphate diphosphohydrolase 1 (NTPDase1)/CD39 is the dominant ectonucleotidase expressed by murine peritoneal macrophages and that it regulates P2X7 -dependent responses in these cells. Macrophages isolated from NTPDase1-null mice (Entpd1,/,) were devoid of all ADPase and most ATPase activities when compared with WT macrophages (Entpd1+/+). Entpd1,/, macrophages exposed to millimolar concentrations of ATP were more susceptible to cell death, released more IL-1, and IL-18 after TLR2 or TLR4 priming, and incorporated the fluorescent dye Yo-Pro-1 more efficiently (suggestive of increased pore formation) than Entpd1+/+ cells. Consistent with these observations, NTPDase1 regulated P2X7 -associated IL-1, release after synthesis, and this process occurred independently of, and prior to, cytokine maturation by caspase-1. NTPDase1 also inhibited IL-1, release in vivo in the air pouch inflammatory model. Exudates of LPS-injected Entpd1,/, mice had significantly higher IL-1, levels when compared with Entpd1+/+ mice. Altogether, our studies suggest that NTPDase1/CD39 plays a key role in the control of P2X7 -dependent macrophage responses. [source] Vascular endothelial growth factor (VEGF)-induced angiogenesis in herniated disc resorptionJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 3 2002Hirotaka Haro Abstract Intervertebral disc herniation is a major cause of low back pain and sciatica. Spontaneous resorption of herniated disc (HD) is frequently detected by magnetic resonance imaging (MRI). Marked infiltration by macrophages and neo-vascularization are observed upon histogical examination of HD. In addition, enhanced MRI studies suggest that HD resorption occurs more frequently in those completely exposed to the epidural space and that this correlates with their degree of vascularization. We have postulated that the angiogenic factor, vascular endothelial growth factor (VEGF), may be implicated in the neo-vascularization of HD tissues. Here we demonstrate that VEGF and its receptors VEGFR-1 and VEGFR-2 are expressed in human surgical samples of HD. Using a co-culture system comprised of murine peritoneal macrophages and intervertebral disc tissue as a model of the acute phase of HD developed previously, an increase in macrophage VEGF protein and mRNA expression was observed upon exposure to disc tissue. Tumor necrosis factor alpha (TNF-,) was required for this induction of VEGF. Use of a novel angiogenesis assay revealed that addition of the conditioned media from the co-culture system resulted in an increase of vascular tubule formation. This effect was strongly inhibited by anti-VEGF antibody, but augmented by recombinant VEGF. We conclude that VEGF induction, under the co-culture conditions tested can result in neo-vascularization of intervertebral disc tissue and may thus play a role in the resorption of HD. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Protein expression changes induced in murine peritoneal macrophages by Group B StreptococcusPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 11 2010Federica Susta Abstract Protein expression changes induced in thioglycolate-elicited peritoneal murine macrophages (M,) by infection with type III Group B Streptococcus (GBS) are described. Proteins from control M, and M, incubated 2,h with live or heat-inactivated GBS were separated by 2-DE. Proteins whose expression was significantly different in infected M,, as compared with control cells, were identified by MS/MS analysis. Changes in the expression level of proteins involved in both positive and negative modulation of phagocytic functions, stress response and cell death were induced in M, by GBS infection. In particular, expression of enzymes playing a key role in production of reactive oxygen species was lowered in GBS-infected M,. Significant alterations in the expression of some metabolic enzymes were also observed, most of the glycolytic and of the pentose-cycle enzymes being down-regulated in M, infected with live GBS. Finally, evidence was obtained that GBS infection affects the expression of enzymes or enzyme subunits involved in ATP synthesis and in adenine nucleotides interconversion processes. [source] | ||||||||||