Disease relevance of NM

• Sepsis is a systemic inflammatory response resulting from local infection due, at least in part, to impaired neutrophil migration [1].
• Endotoxemia enhances expression of the signaling receptor (GP130) on protein and molecular level [2].
• Multiple myeloma and B cell lymphoma. Investigation of IL-6, IL-6 receptor antagonist (IL-6RA), and GP130 antagonist (GP130A) using various parameters in an in vitro model [3].
• Alpha-1-antitrypsin (A-1-AT) and A-1-AT-elastase complex levels in cerebrospinal fluid have been evaluated in 11 children with viral meningitis (VM), 14 with bacterial meningitis (BM), 10 with tuberculous meningitis (TBM) and 10 investigated for, but found not to have meningitis (NM) [4].
• Each prognostic marker was determined independently and without the knowledge of clinical features and outcome by different investigators in 275 (HG), 96 of 275 (DI), 94 of 275 (NM), and 224 of 275 patients (LDH) with neuroblastoma by methods described previously [5].

Psychiatry related information on NM

• Numerous examples of such biphasic responses were documented, including osteoclast differentiation, various vascular responses, neutrophil migration, superoxide anion formation, exploratory behavior in rodents, vitamin D3 levels in macrophages, human sperm motility and mobility, myocardial contraction, and other functions [6].
• In the plaice (Pleuronectes platessa L.), the serum concentration of lysozyme and the acute phase reactant, C-reactive protein (CRP) and in vitro neutrophil migration have been used as indicators of the ability of test substances to modulate nonspecific defense mechanisms [7].

High impact information on NM

• Although annexins lack signal sequences for secretion, some members of the family have also been identified extracellularly where they can act as receptors for serum proteases on the endothelium as well as inhibitors of neutrophil migration and blood coagulation [8].
• Neutrophil turnover increased almost four-fold (P = 0.005), whereas neutrophil migration to a skin chamber was normal [9].
• Neutrophil migration into skin lesions ranged from 34 to 469 x 10(5) cells per day in the lithium-treated patients, as compared with 1.7 to 68 x 10(5) in 10 controls [10].
• The peptide inhibited neutrophil migration on vitronectin by interfering with the release of the cells from sites of attachment [11].
• Regulation of transendothelial neutrophil migration by endogenous interleukin-8 [12].

Chemical compound and disease context of NM

• Abnormalities in neutrophil migration detected in a chemical peritonitis model are likely secondary to abnormal CD11b integrin and L-selectin expression on C/EBPepsilon-deficient neutrophils [13].
• Peptides that bound to the alpha(M) integrin-I domain and inhibited its complex formation with proMMP-9 prevented neutrophil migration in a transendothelial assay in vitro and in a thioglycolate-elicited peritonitis in vivo [14].
• Directed neutrophil migration to IL-8 is increased in cystic fibrosis: a study of the effect of erythromycin [15].
• Effect of ibuprofen on neutrophil migration in vivo in cystic fibrosis and healthy subjects [16].
• Scavenging of reactive nitrogen species (e.g. peroxynitrite) inhibits neutrophil migration and joint hyperalgesia in the acute phase of zymosan arthritis in rats [17].

Biological context of NM

• The results suggested that the decreased expression of GP130 in ejaculated spermatozoa could be associated with low sperm motility in asthenozoospermic men [18].
• The inability of IL-12(-/-) mice to restrict the infection was not due to impairment of neutrophil migration, but correlated with decrease of phagocytosis, NO production, and microbicidal activities of their neutrophils, and with reduction of systemic IFN-gamma synthesis [1].
• A statistically significant association of low HG (1 and 2) was found with DI of more than 1 (hyperdiploid), single copy of NM gene per haploid genome, and an LDH of less than 1500 IU/l (P value for each, < 0.001), factors that are associated with better prognosis [5].
• Neutrophil migration inhibitory properties of polyunsaturated fatty acids. The role of fatty acid structure, metabolism, and possible second messenger systems [19].
• Structural analysis of human neutrophil migration. Centriole, microtubule, and microfilament orientation and function during chemotaxis [20].

Anatomical context of NM

• IL-12 acts through induction of IFN-gamma and stimulation of phagocytic and microbicidal activities of neutrophils, rather than neutrophil migration per se [1].
• The avian cochlear nucleus, n. magnocellularis (NM), makes bilateral projections to its target, n. laminaris (NL) [21].
• Neutrophil migration inhibition factor from T lymphocytes (NIF-T) is a lymphokine that acts to localize granulocytes [22].
• Neutrophil migration across mucosal epithelium during inflammatory episodes involves the precise orchestration of a number a cell surface molecules and signaling pathways [23].
• Neutrophil migration into the inflamed peritoneal cavity was severely inhibited in IL-8 transgenic mice, but not in nontransgenic littermates [24].

Associations of NM with chemical compounds

• Fibrin regulates neutrophil migration in response to interleukin 8, leukotriene B4, tumor necrosis factor, and formyl-methionyl-leucyl-phenylalanine [25].
• The integrin alpha9beta1 mediates adhesion to activated endothelial cells and transendothelial neutrophil migration through interaction with vascular cell adhesion molecule-1 [26].
• The antagonists WEB 2086 and L-652,731 had no effect on neutrophil migration across resting EC induced by formylmethionyl-leucyl-phenylalanine (FMLP) [27].
• Identification of hepoxilin A3 in inflammatory events: a required role in neutrophil migration across intestinal epithelia [28].
• PAF-enhanced CD18 expression on neutrophils and neutrophil migration were both abolished by L658 758 but PAF-induced neutrophil adhesion to endothelial monolayers was not affected by the antiproteinase [29].

Physical interactions of NM

• No evidence of neutrophil migration was observed towards purified complex derived from equine neutrophil elastase and the Spi 1 isoform of equine API, or to crude mixtures of porcine pancreatic elastase and unseparated equine API isoforms, although the same neutrophil preparations actively migrated towards zymosan activated plasma [30].
• Sera obtained from patients with rheumatoid arthritis with evidence of circulating immune complexes were able to significantly inhibit neutrophil migration, indicating that this phenomenon may be a useful means for the detection of circulating immune complexes [31].
• The results also suggest that neutrophil migration induced by KM+ involves binding to CXCR2 [32].

Enzymatic interactions of NM

• Role of interleukin-8 phosphorylated kinases in stimulating neutrophil migration through fibrin gels [33].

Regulatory relationships of NM

• Identification of a potent, selective non-peptide CXCR2 antagonist that inhibits interleukin-8-induced neutrophil migration [34].
• Inhibition of IL-8 and TNF-alpha production by acute EtOH intoxication may inhibit inflammatory focused neutrophil migration and activation and may be a mechanism explaining the increased risk of trauma- and burn-related infections [35].
• Studies of neutrophil migration across filters without endothelium showed that migration was promoted in the presence of a gradient of either CSF, but was equally promoted against the gradient; that is, the CSFs are chemokinetic but not chemotactic [36].
• On the other hand, no neutrophil migration was induced by IL-13, even at 1 microM concentrations [37].
• Conditioned medium from IL-1 beta-exposed HT-29 cells stimulated neutrophil migration (395% of control, P < 0.01), and this effect was completely inhibited by anti-IL-8 antibody [38].

Other interactions of NM

• A-1-AT concentrations in the NM group were lower than in the BM group (P = 0.0002) and the TBM group (P = 0.0005) but did not differ from the concentrations in VM; those in the VM group were lower than in the BM group (P = 0.0001) and the TBM group (P = 0.003) but no difference was found between the BM and TBM groups [4].
• Further analysis showed that this antibody recognized CD47, a ubiquitously expressed plasma membrane protein previously implicated in integrin function, host defense action, and neutrophil migration [39].
• We recently reported that heme is a proinflammatory molecule, able to induce neutrophil migration, reactive oxygen species generation, and IL-8 expression [40].
• TNF-alpha, a proinflammatory cytokine, initiates expression of endothelial cell surface adhesion molecules and neutrophil migration. p38, a member of the mitogen-activated protein kinases, plays an important role in mediating intracellular signal transduction in endotoxin-induced inflammatory responses [35].
• Supernatants of the VEGF/VPF-treated HBMECs significantly increased neutrophil migration across the HBMEC monolayer compared with those of the untreated control [41].

Analytical, diagnostic and therapeutic context of NM

• The protein expression of GP130 was further confirmed by both immunocytochemistry and Western blot [18].
• With RT-PCR, only GP130 mRNA but not IL-6 and IL-6R mRNA was expressed in human ejaculated spermatozoa [18].
• These interactions lead to neutrophil adherence to the endothelium, neutrophil migration into the underlying tissues, and subsequent tissue injury (e.g. myocardial reperfusion injury).(ABSTRACT TRUNCATED AT 400 WORDS)[42]
• Neutrophil migration is defective during recombinant human granulocyte-macrophage colony-stimulating factor infusion after autologous bone marrow transplantation in humans [43].
• In addition, intraperitoneal injection of IL-17B purified from Chinese hamster ovary cells caused marked neutrophil migration in normal mice, in a specific and dose-dependent manner [44].

References