Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement C5”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources
PubMed1989

Role of complement-derived and bacterial formylpeptide chemotactic factors in the in vivo migration of neutrophils in experimental Escherichia coli pyelonephritis in rats.

In experimental Escherichia coli pyelonephritis, the bacterial multiplication in the kidney parenchyma triggers a burst of neutrophil extravascular migration, as measured by the myeloperoxidase (MPO) activity in the kidney, a marker for tissue neutrophil infiltration. To test the mechanisms of in vivo neutrophil migration, pyelonephritis was surgically induced in rats that were then either complement-depleted with cobra venom factor (CVF), resulting in a profound hypocomplementemia for 72 h after inoculation, or treated with phenylbutazone (PB), a competitive antagonist of bacterial chemotactic formylpeptides. Compared to controls, CVF- and PB-treated animals killed when the neutrophil infiltration started (32 h) had a significantly reduced neutrophil infiltration, as measured by kidney MPO activity. This effect disappeared in animals killed 72 h after surgery, when neutrophil infiltration peaked. These data suggest that redundant chemotactic mechanisms triggered neutrophil migration. Inhibiting one of these mechanisms only transiently delayed neutrophil migration but did not affect the peak infiltration.

Animals↗
PubMed2005

Novel delivery of oligonucleotides using a topical hydrogel tissue sealant in a murine partial nephrectomy model.

PURPOSE: Ischemia/reperfusion injury is a leading cause of renal damage and antisense gene therapy has been shown to ameliorate its effects. However, this approach has been limited by current delivery methods that require high concentrations of intravenous nucleic acids lacking specificity for targeting tissues. To overcome these limitations we developed a novel murine partial nephrectomy model to evaluate polyethylene-glycol (PEG) hydrogel tissue sealant as a topical oligonucleotide delivery system. MATERIALS AND METHODS: A total of 18 male C57BL/6 mice underwent left partial nephrectomy with vascular occlusion. Hydrogel primer and then sealant were applied to the cut surface and photopolymerized. Using this method 16 additional mice received hydrogel primer mixed with Cy5 labeled fluorescent oligonucleotide (10 to 100 microg). Kidneys were harvested at various time points and assessed for oligonucleotide penetration using fluorescence microscopy. RESULTS: A survival rate of 100% (34 subjects) was obtained using this mouse model of partial nephrectomy. PEG hydrogel provided adequate protection against renal hematoma and intraperitoneal blood. Fluorescent images revealed that 50 microg was the minimum dose resulting in complete progressive cellular penetration with time. In addition to direct diffusion from the application site, movement of oligonucleotide through the subcapsular space into the cortex was an observed mechanism of distribution. CONCLUSIONS: A murine partial nephrectomy model was successfully created using PEG hydrogel. In addition to achieving hemostasis, hydrogel served as a successful depot for delivering oligonucleotides throughout the kidney.

Animals↗
PubMed1994

Protection elicited by a replication-defective adenovirus vector expressing the tick-borne encephalitis virus non-structural glycoprotein NS1.

Tick-borne encephalitis virus (TBEV) encodes a conserved, immunogenic, non-structural protein NS1 that is glycosylated and secreted from infected cells in an oligomeric form. An adenovirus recombinant, RAd51, expressing high levels of TBEV NS1 has previously been demonstrated to protect mice against a lethal challenge with TBEV. We show here that BALB/c mice infected with TBEV experienced a transient viraemia between days 3 to 5 post-inoculation that was detectable prior to the encephalitic phase of infection. Mice vaccinated with RAd51 were protected against both the viraemic and encephalitic infections associated with the TBEV challenge. Protection was demonstrated to be due to NS1 synthesized de novo from RAd51 in the vaccinated mice. Since TBEV NS1 is expressed on the cell surface, antibody-dependent complement-mediated cytolysis (CMC) of infected cells was considered as a possible mechanism of protection. Vaccination with the recombinant adenovirus proved to be effective in a mouse strain carrying a genetic deletion in the complement receptor C5. CMC is therefore not an essential component of the observed protective immune response.

Adenoviridae↗
PubMed1983

Hypercatabolism of complement in Crohn's disease--assessment of circulating C3c.

Split products from the main complement component 3 (C3) were investigated in untreated outpatients, 20 with Crohn's disease and 20 with ulcerative colitis. The median plasma concentration of c split product of C3 (C3c) in normals was 2 mg X 1(-1), in patients with Crohn's disease 20 mg X 1(-1) and in patients with ulcerative colitis 3 mg X 1(-1). This tenfold increase in C3c was significant at the 0.005-level. Plasma C3c exceeded the reference interval in two patients with ulcerative colitis. C3c levels did not correlate to the activity of the disease or to the occurrence of the C3 phenotypes S, FS and F. Substantially elevated plasma C3c in Crohn's disease suggests hypercatabolism of C3, that is, involvement of complement reactions. Further studies are needed to reveal the site of cascade activation and to define the role of complement for the pathogenesis of the disease.

Colitis, Ulcerative↗
PubMed2004

Cryptococcal capsular glucuronoxylomannan reduces ischaemia-related neutrophil influx.

BACKGROUND: The capsular polysaccharide glucuronoxylomannan (GXM) of Cryptococcus neoformans interferes with the chemotaxis and transendothelial migration of neutrophils. Intravenous administration of purified GXM has been shown to reduce the influx of inflammatory cells in an animal model of bacterial infection. Here we show that isolated GXM can also interfere with neutrophil migration in a model of inflammation not related to infection. We assessed the effects of intravenous GXM on neutrophil infiltration in a rat model of myocardial ischaemia, where neutrophil infiltration has been shown to contribute to postischaemic reperfusion injury. MATERIALS AND METHODS: Rats were subjected to coronary artery ligation followed by a 3-h reperfusion period. Myeloperoxidase-activity was measured in the ischaemic tissues as a marker of neutrophil infiltration. RESULTS: Intravenous administration of GXM markedly reduced the influx of neutrophils in the ischaemic myocardium as measured by a 65% reduction of tissue MPO activity. This reduction of MPO activity was clearly correlated to the serum concentration of GXM. As complement activation by GXM was minimal at the doses applied in vivo, it is unlikely that generation of chemotactic C5a in the circulation by GXM caused the observed reduction in leucocyte migration. CONCLUSION: Purified cryptococcal GXM has the ability to reduce neutrophil influx even outside the scope of infection.

Animals↗
PubMed1977

C1 subcomponents in acute pneumococcal otitis media in children.

Twenty children with acute pneumococcal otitis media were studied. In 6 children the infection ran a normal course and healed after the first episode and in 14 it relapsed. The serum levels of the immunoglobulins IgG, IgA and IgM were normal in all 20 children. Specific antibodies to pneumococcal polysaccharide were found in all cases, with no differences in the titers between the relapsed cases and those that healed. The complement components were quantitated with electroimmuno assay. G1q proved depressed in 60 per cent of the relapsed cases and in 16 per cent of the healed cases. C1r and C1s were disproportionally high compared with the C1q levels. Furthermore, crossed immunoelectrophoresis revealed abnormal complexes composed of C1r and C1s, and complexes composed of C1r, C1s and C1 IA. These complexes were more pronounced in sera from the children with relapsing otitis media.

Acute Disease↗
PubMed1982

Therapeutic ramifications of the interaction of complement, granulocytes, and platelets in the production of acute lung injury.

Evidence is reviewed that activation of complement through its ability to cause adhesion of granulocytes to the pulmonary endothelium (margination) and aggregation and embolization of these cells to the lung microvasculature is an important cause of pulmonary injury. Agents capable of diminishing such stimulated adhesiveness might be rational therapeutic adjuncts in vascular-damaging syndromes and are being investigated. To date, corticosteroids, such as methylprednisolone (in enormous doses), and certain nonsteroidal anti-inflammatory drugs, such as ibuprofen, have been shown to diminish granulocyte stickiness in vitro and diminish complement-mediated tissue damage in vivo. Moreover, platelets amplify complement/granulocyte-induced endothelial damage by releasing serotonin, which, in turn, potentiates granulocyte adhesion to endothelium. This potentiation is abrogated by the serotonin antagonists imiprimine and methysergide. Since these diverse agents inhibit granulocyte-adhesion phenomena by different mechanisms, they might predictably be synergistic in their beneficial effect. This prediction is validated for methylprednisolone and ibuprofen, for which we report a threefold synergism in preventing complement-mediated granulocyte aggregation in vitro. Preliminary studies indicate utility of this synergism in vivo as well, in that the degree of myocardial infarction [a complement-activating phenomenon) is diminished in coronary-ligated animals in which rather small doses of the two drugs administered together.

Adrenal Cortex Hormones↗
PubMed1970

Inflammation and herpes simplex virus: release of a chemotaxis-generating factor from infected cells.

Infection of primary rabbit kidney cells with herpes simplex virus leads to the release of a cell factor or factors that upon incubation with serum results in the cleavage of the fifth component, C5, of complement. The product of this cleavage, C5a, is chemotactic for polymorphonuclear leukocytes and could be responsible for the accumulation of these cells at the site of herpetic lesions.

Animals↗
PubMed1984

Nicotine is chemotactic for neutrophils and enhances neutrophil responsiveness to chemotactic peptides.

Neutrophils contribute to chronic bronchitis and pulmonary emphysema associated with cigarette smoking. Nicotine was found to be chemotactic for human neutrophils but not monocytes, with a peak activity at approximately 31 micromolar. In lower concentrations (comparable to those in smokers' plasma), nicotine enhanced the response of neutrophils to two chemotactic peptides. In contrast to most other chemoattractants for neutrophils, however, nicotine did not affect degranulation or superoxide production. Nicotine thus may promote inflammation and consequent lung injury in smokers.

Chemotaxis, Leukocyte↗