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At least 235 records · Page 13Linked to original sources
PubMed2005

Helicobacter pylori eradication decreases the expression of glycosylphosphatidylinositol-anchored complement regulators, decay-accelerating factor and homologous restriction factor 20, in human gastric epithelium.

BACKGROUND: It has previously been reported that there is a strong correlation between the expression of glycosylphosphatidylinositol (GPI)-anchored complement membrane inhibitor in gastric epithelium and the severity of inflammation of gastric mucosa. To investigate the regulation of complement activity in gastric epithelium during Helicobacter pylori (H. pylori)-associated gastritis, the expression of GPI-anchored complement membrane inhibitors, decay-accelerating factor (DAF) and 20-kDa homologous restriction factor 20 (HRF20), and membrane cofactor protein (MCP), which is a transmembrane protein, were evaluated after removal of the H. pylori stimulus. Furthermore, the expression of the complement fragment, C3c, was also investigated. METHODS: Forty-six patients with epigastric symptoms and endoscopically confirmed peptic ulcer or gastritis who had H. pylori infection of the gastric mucosa were enrolled in the present study. Biopsy specimens were obtained from the gastric antrum and corpus 1 month before and after eradication. Helicobacter pylori infection was determined by the rapid urease test, histology, and culture before eradication, and by histology, culture, and urea breath test after eradication. Gastric biopsy specimens obtained before and after eradication were evaluated for infiltration by neutrophils and mononuclear cells. The expression of complement membrane inhibitors, DAF, HRF20, and MCP and that of the main complement fragment, C3c, was immunohistochemically evaluated. RESULTS: One month after the eradication of H. pylori, the infiltration by neutrophils and mononuclear cells in the gastric mucosa decreased significantly (P < 0.0001) as compared with that before eradication. The expression of DAF, HRF20, and C3c on gastric mucosal epithelium also significantly decreased in both the antrum and the corpus (P < 0.05) 1 month after eradication. However, no change was observed in the expression of MCP. CONCLUSIONS: The decrease in the expression of GPI-anchored complement regulator and the complement after removal of a chronic microbial stimulus suggests that the gastric epithelium appears to undergo an aggressive stress of complement during H. pylori infection. Conclusively, DAF and HRF20 may play an important protective role against complement-mediated damage induced by chronic microbial stimuli in such a pathological condition.

Amoxicillin↗
PubMed1986

C1 esterase inhibitor deficiency in X-linked hypogammaglobulinaemia: an anomaly fostering anaphylactoid reactions following intramuscular gammaglobulin administration.

A patient with apparent X-linked agammaglobulinaemia was found to be inordinately susceptible to anaphylactoid reactions to intramuscular injections of gammaglobulin. The patient was found also to have low levels of C1 esterase inhibitor (C1 INH). The possibility that the C1 INH deficiency and in this patient, whether genetic or acquired, fostered the susceptibility to the production of anaphylactoid reactions after gammaglobulin injections urges further studies of the association of C1 INH deficiency and anaphylactoid reactions to gammaglobulin injections. The possibility that C1 INH levels like C1q levels may be low in hypogammaglobulinaemic patients as a consequence of increased catabolism of this regulator of the complement system when IgG levels are low is considered.

Adult↗
PubMed1999

Inhibition of a membrane complement regulatory protein by a monoclonal antibody induces acute lethal shock in rats primed with lipopolysaccharide.

Rats pretreated with traces of LPS developed acute fatal shock syndrome after i.v. administration of a mAb that inhibits the function of a membrane complement regulatory molecule. Such a shock was not observed after the administration of large amounts of LPS instead of the mAb following LPS pretreatment. The lethal response did not occur in rats depleted of either leukocytes or complement, and a C5a receptor antagonist was found to inhibit the reaction. Furthermore, LPS-treated rats did not suffer fatal shock following the injection of cobra venom factor, which activates complement in the fluid phase so extensively as to exhaust complement capacity. Therefore, complement activation on cell membranes is a requirement for this type of acute reaction.

Acute Disease↗
PubMed2002

Recurrent pneumococcal meningitis in homozygous C3 deficiency.

Congenital deficiencies of complement system proteins are rare. A 4-year-old girl was admitted for meningitis. She had had repeated attacks of pneumococcal meningitis and otitis media at the age of 3 years. Analysis of cerebrospinal fluid showed that this meningitis was due to pneumococcal infection. Complement 3 and CH50 values of the proband and her brother were low, while her parents were normal. The patient was given polyvalent pneumococcal and anti-haemophilus vaccines plus ceftriaxone. Recovery was complete after 15 days of antibiotic therapy. This is the first description of a case of recurrent meningitis with C3 and CH50 deficiency in a Turkish family.

Child, Preschool↗
PubMed1990

[Method of determining functional age from the aspect of immunologic markers of aging].

In a series of 310 subjects partial functional immunochemical age was determined by the method of multivariant linear regression. The authors suggested equations for the determination of partial functional immunochemical age, separately for men, women, and mixed groups, as well as for the determination of global functional age by using parameters of other systems of the body. A possible correction of the equations is discussed with the aim to eliminate the phenomenon of distorted results in the extreme positions of the chronological age axis. The contribution of the method of assessing partial functional immunological age to the selection of relevant markers of aging of the immune system is substantiated and its importance in justifying geroprotective and therapeutic procedures is emphasized.

Adult↗
PubMed1994

Expression of complement-regulatory proteins in normal and UW-preserved human liver.

BACKGROUND/AIMS: Somatic cells are protected against complement-mediated injury by specialized membrane proteins, known as complement-regulatory proteins (CRP). The knowledge of the pattern of CRP expression in the liver is important to evaluate the role of complement-mediated injury in graft rejection. METHODS: We determined the distribution of four main CRP: membrane cofactor protein (MCP), decay accelerating factor (DAF), protectin, and complement receptor 1 (CR1) in 30 histologically normal livers, 13 samples from University of Wisconsin cold-storage solution (UW)-preserved tissue and 17 postoperative biopsies of UW-preserved allografts. RESULTS: In normal liver, hepatocytes expressed only MCP. Bile duct cells were reactive for MCP and protectin. Sinusoidal endothelial cells expressed MCP and protectin but displayed no or faint expression of DAF. Endothelial cells of portal vessels and centrilobular veins expressed high levels of DAF, MCP, and protectin. No expression of CR1 was observed. No change in CRP expression was usually detected after UW preservation, except for protectin, induced on hepatocytes in 9 samples of UW-preserved liver tissue and in 9 allografts. CONCLUSIONS: Hepatocytes and sinusoidal endothelial cells, which have a defective expression of CRP, might be at risk for complement-mediated injury. However, this risk is not aggravated after UW preservation.

Adenosine↗
PubMed1983

Complement-like activity in sea urchin coelomic fluid.

A complement-like activity in echinoid coelomic cell-free fluid is described. The activity is detected by the lytic action on rabbit erythrocytes (RRBC), and by the opsonic effect on echinoid coelomic phagocytes and mouse peritoneal macrophages. This activity is very heat-labile, being completely destroyed at 37 degrees C 1/2 hr, and is inhibited by Ca2+ concentrations below 10 mM and by low pH. Lysis was complete within 3-4 min, and the titer (10(7) RRBC/ml) was 20-60 between animals. Various substances known to inhibit human complement also inhibited the lytic and opsonic activities in echinoid fluid. RRBC opsonized with echinoid fluid were attached to mouse macrophages without being internalized, an effect which resemble complement opsonization. It is concluded that an activity is present in echinoid coelomic fluid, which strongly resembles mammalian complement activated via the alternative pathway. A lectin-like activity with specificity for D-fucose was detected by the agglutination of RRBC (titer 300-600). Hemagglutination was inhibited by sugars which did not inhibit the lytic and opsonic process. On the other hand, hemagglutination was resistant to various physio-chemical treatments which led to inactivation of the complement-like system; thus these two activities seem to be unrelated. The lectin-like activity did not mediate any opsonic effect.

Animals↗
PubMed1989

The role of complement in the pathogenesis of experimental allergic encephalomyelitis.

The role of complement in the pathogenesis of demyelination and inflammation has been investigated in a synergistic model of acute experimental allergic encephalomyelitis (EAE) in the Lewis rat. Depletion of serum complement with cobra venom factor (CVF) suppressed the clinical expression of acute inflammatory EAE induced either by immunization with 50 micrograms guinea pig basic protein (MBP) in Freund's complete adjuvant, or by the passive transfer of 10(7), but not 5 X 10(7) MBP activated spleen cells. Despite the suppression of clinical disease in actively induced EAE, treatment with CFF only had a significant effect on the severity of CNS inflammation in early disease (12 days postimmunization) when the number of inflammatory foci was reduced by 35%. Three days later this difference had resolved and no significant difference could be detected in the severity of CNS inflammation, although control animals exhibited severe disease, the CVF treated group being clinically normal. Demyelination in these models is initiated by systemic injection of the antimyelin oligodendrocyte glycoprotein (MOG) monoclonal antibody, 8-18C5, which in vitro lyses oligodendrocytes in a dose, Fc and complement-dependent manner and in vivo induces extensive CNS demyelination in rats with EAE. Treatment with CVF reduced the ability of this antibody to initiate demyelination in vivo and furthermore, its F(ab)2' fragment had no effect on the clinical course of EAE and was unable to initiate demyelination in normal animals. Complement-dependent mechanisms are therefore involved both in the clinical expression of acute inflammatory lesions and in the pathogenesis of antibody-mediated demyelination in EAE.

Animals↗