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PubMed2005

Intravenous immunoglobulin attenuates mesenteric ischemia-reperfusion injury.

Intravenous immunoglobulin (IVIG) has been found useful in the treatment of various clinical entities and its effect has been associated with inhibition of complement-mediated tissue damage. The aim of this study was to determine the ability of IVIG to protect against mesenteric ischemia-reperfusion (IR)-induced local and remote injury. Rats received vehicle or IVIG (150-600 mg/kg) 5 min prior to sham operation or 30 min of superior mesenteric artery occlusion, followed by 5, 120, or 240 min of reperfusion. IVIG reduced IR-induced mucosal injury without altering IR-induced increases in PMN infiltration or LTB(4) generation. At 5 min post IR, the deposition of IgG and C3 in the lamina propria and surface epithelial cells was attenuated by IVIG. The increased capillary leak, evident at 240 min, was inhibited by IVIG and coincided with a reduction in C3 deposition in lung tissue. The beneficial effects of IVIG may be related to the ability to scavenge deleterious products.

Animals↗
PubMed2004

Relapsing polychondritis, induced in mice with matrilin 1, is an antibody- and complement-dependent disease.

Relapsing polychondritis is an autoimmune disease that affects cartilage in the ear, nose, and respiratory tract. A pathogenic immune response has been proposed and antibodies to several cartilage proteins are detected in sera from these patients. To investigate the role of the humoral immune response in relapsing polychondritis, we used the matrilin-1-induced relapsing polychondritis model. Mice deficient of B cells (muMT) and mice congenic at the complement factor 5, were immunized with matrilin-1, a cartilage-specific protein mainly detected in the tracheal cartilage. To investigate the binding properties and tissue selection of matrilin-1-specific antibodies we produced matrilin-1-specific B-cell hybridomas. Although 83% of the micro MT heterozygous mice developed respiratory distress and erosive chondritis in the respiratory tract, none of the B-cell-deficient mice were susceptible to disease. In addition, we show that complement factor 5 is important for the induction of matrilin-1-induced relapsing polychondritis. Monoclonal matrilin-1-specific antibodies injected into neonatal mice bound specifically to cartilage of the respiratory tract and adult B-cell-deficient mice injected with the same antibodies developed erosive chondritis in the respiratory tract. We conclude that relapsing polychondritis can be mediated by a pathway involving tissue-specific antibodies and complement activation.

Animals↗
PubMed1980

Preparation of an R3 reagent (serum depleted of the third component of human complement (C3)) by immunoadsorption. Application to the hemolytic assay of human C3.

We have devised a simple one-step preparation of C3 depleted serum (R3). Fresh normal human serum, with complement activation inhibitors, was depleted of C3 by affinity chromatography on a Sepharose anti-C3c. To prevent non-specific interactions, a high ionic strength buffer containing saccharose was used. Immunochemical analysis and complement activity assays demonstrate that this C3 depleted serum is a suitable R3 reagent. This R3 reagent has been used successfully for titration of hemolytic activity of C3 in normal and abnormal sera. Two simple, specific and sensitive assays are described.

Animals↗
PubMed2003

Xenogeneic direct hemoperfusion using whole swine liver for liver failure in dogs.

BACKGROUND: We developed a new method of xenogeneic direct hemoperfusion of a bioartificial liver support system consisting of a leukocyte-adsorbent column, an immunoglobulin-adsorbent column, and the substitute unit for hepatic function. By this method, we performed xenogeneic direct hemoperfusion experiment using resected whole swine liver for treatment of a canine liver failure model, and compared the contribution of each adsorbent column both by blood analysis and from the histological point of view. MATERIALS AND METHODS: Canine liver failure model was produced by portocaval shunting and ligating the entire hepatoduodenal ligament. The xenogeneic direct hemoperfusion system was constructed using a roller pump, a leukocyte-adsorbent column, an immunoglobulin-adsorbent column, a combined device of oxygenator and warmer, the resected whole swine liver accommodated in a chamber, and a dissolved oxygen meter through which canine whole blood leaving the external jugular vein circulated in this order. RESULTS: Xenogeneic direct hemoperfusion was successfully performed for 3 h without hyperacute rejection occurring. Adequate ammonia detoxification and bile juice secretion were exhibited, and no findings of hepatocyte destruction by immunological cells and proteins were detected. Blood data showed that the immunoglobulin adsorbent were more effective than the leukocyte adsorbent in avoiding hyperacute rejection. This result indicates that hyperacute rejection has a closer relation to humoral immune responses, especially regarding removal of complements than to cellular immune responses. CONCLUSIONS: We successfully performed xenogeneic direct hemoperfusion of the whole swine liver without hyperacute rejection using our method.

Adsorption↗
PubMed1980

Childhood neutropenia.

Neutropenia can occur because of abnormalities of marrow stem cell development, poor release of polymorphonuclear leukocytes from the marrow reserve, or decreased survival of polymorphonuclear leukocytes. Some of the more important clinical entities are discussed.

Aging↗
PubMed1980

Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome. Pathophysiological relevance and possible prognostic value.

Clinical and experimental observations suggest that aggregation of polymorphonuclear granulocytes (PMN) in response to activated complement (C) might contribute to the genesis of the adult respiratory distress syndrome (ARDS), aggregating PMN causing pulmonary dysfunction by becoming lodged in the lung as leucoemboli. PMN-aggregating activity can be detected in C-activated plasma and reflects C5a levels. In 61 patients at risk for ARDS a strong and highly significant correlation was found between the presence of PMN-aggregating activity in the plasma and the development of ARDS; this correlation was also significant when patients with sepsis were excluded from analysis. In patients followed prospectively detection of elevated C5a seemed to be a useful predictor of ARDS. Since corticosteroids have been shown to inhibit PMN aggregation both in vitro and in vivo, the evidence for a role for PMN aggregation in the genesis of ARDS supports the use of corticosteroids in this disorder.

Cell Aggregation↗
PubMedDate not supplied

Identification of a homologue of CD59 in a cyclostome: implications for the evolutionary development of the complement system.

We have employed a COS cell expression cloning procedure to isolate a full length cDNA clone encoding a hagfish leukocyte-associated membrane protein (HLMP1). The protein, which is identified by a monoclonal antibody (JB3) generated in our laboratory, is present on the majority of hagfish leukocytes and is also expressed on erythrocytes. The cDNA clone contained an open reading frame encoding a 120 residue polypeptide which exhibits 33% amino acid sequence identity with the precursor protein of human CD59, a leukocyte-associated membrane protein which regulates the action of the complement membrane attack complex on homologous cells. CD59 belongs to a family of structurally related glycoproteins which includes the Ly-6 proteins expressed on mouse lymphocytes. In addition to significant overall sequence homology HLMP1 shows conservation of 8 key cysteine residues with members of the CD59/Ly-6 family. Comparison of the hagfish sequence with that of the mature human CD59 protein suggested a processed protein consisting of 74 amino acids associated with the cell membrane via a GPI anchor. The latter was confirmed by immuno-flow cytometry following treatment of transfected COS cells with phospholipase. Phylogenetic analysis and tissue distribution of this protein in the hagfish are consistent with HLMP1 being a homologue of CD59. A three-dimensional model of HLMP1, constructed using the NMR-determined structure for human CD59 as a template, indicated conservation of a core structure of five strands of beta-sheet and a short helix stabilised by four disulfide bonds. These findings, when taken together with our previous identification of C5a-like chemotactic activity in LPS-activated serum, provide indirect evidence for the existence of the terminal lytic complement pathway (C5 to C9) in these primitive vertebrates.

Animals↗
PubMed1983

C5a-induced chemiluminescence of human granulocytes and its amplification by a serum factor.

Purified human C5a elicits a fast chemiluminescence (CL) response from isolated human granulocytes in the presence of Lucigenin (bis-N-methylacridinium nitrate). The reaction is inhibitable to more than 90% by superoxide dismutase (SOD) - final concentration 200 micrograms/ml -, to about 60% by catalase - final concentration 10 mg/ml - and to 30% by the hydroxyl radical scavenger D-mannit - final concentration 100 mM. Therefore O2- seems to be the oxygen radical responsible for most of the CL, while OH and H2O2 are also involved. Addition of normal pool serum to the cells for 1-2 min before stimulation with C5a strongly enhances the effect in a dose and time-dependent manner. Therefore the existence of a "helper activity" in serum amplifying the C5a-induced CL of granulocytes is postulated. This "helper activity" is, however, no specific for C5a, since CL responses elicited with the chemotactic peptide f-met-phe or by phorbol-myristate-acetate (PMA) are also enhanced by preincubation with serum. In contrast, ConA-induced CL is not enhanced but decreased. Therefore, though not unique to C5a-induced CL, the "helper activity" seems not to represent a general "adjuvans" effect of serum on the granulocytes, but to be restricted to certain stimuli.

Chemotaxis, Leukocyte↗
PubMed1987

C5a-specific modulation of phagocyte functions in patients with localized bacterial infections.

Chemotaxis, enzyme release and superoxide-anion (O2-) generation of purified peripheral blood neutrophils (PMN) and monocytes were studied in a total of 87 patients suffering from localized bacterial infections. Shortly after disease onset, single or several PMN functions became non-responsive to the complement split product C5a. Functional activities elicited by the synthetic peptide f-met-leu-phe or leukotriene B4 remained unaltered. C5a-specific impairment lasted one to several days and returned to normal with the subsidence of the disease. C5a elicited release of beta-glucuronidase as well as generation of superoxide-anions was seen more often to be impaired as compared to chemotactic migration. In contrast to PMN, monocytes from the same patients failed to show paralleling C5a-specific functional alterations. There was no correlation between impairment of PMN functions and plasma levels of the complement split-products C3a and C4a as determined by RIA. It is concluded that in acute infectious disease a graded C5a-specific modulation of PMN functions may be present. This phenomenon is transient and not paralleled by functional alterations of monocytes or changes in plasma complement levels.

Bacterial Infections↗
PubMed2001

Massive muscle cell degeneration in the early stage of merosin-deficient congenital muscular dystrophy.

Primary merosin-deficient congenital muscular dystrophy (CMD) is a severe form of congenital muscular disorder which is caused by mutations in the laminin alpha2 chain gene (LAMA2). The disease is characterized by marked dystrophic changes in skeletal muscles during early infancy, while little is known about the pathological process of the muscle fiber degeneration. Here, we report the immunohistochemical analysis of skeletal muscle in ten patients with primary merosin-deficient CMD using a panel of molecular markers for skeletal muscle proteins, cellular necrosis, and apoptosis. In the youngest patient (a 52 day old baby), prominent massive muscle cell degeneration occurred in association with the deposition of the C5-9 complement membrane attack complex (MAC). Most of the MAC-positive muscle fibers showed a severely deranged immunoreaction to dystrophin, dystroglycans, and other sarcolemmal proteins. In addition, we found scattered positive signals for apoptosis. Similar but milder changes were also observed in six other patients younger than 1 year. In the patients older than 3 years, muscle fibers positive for MAC and apoptotic signals were barely detectable. These findings imply that massive muscle fiber degeneration occurs in the very early stage of merosin-deficient CMD and may contribute to the severe dystrophic changes in muscle from early infancy.

Biopsy↗
PubMed2004

Activation of complement and leukocyte receptors during on- and off pump coronary artery bypass surgery.

OBJECTIVE: The aim of this prospective, randomised study was to investigate the influence of extracorporeal circulation on the inflammatory response, our hypothesis being that off pump coronary artery bypass grafting (OFFCAB) procedures would generate less activation than on pump procedures (ONCAB). METHODS: Patients admitted for elective CABG were randomised to either ONCAB or OFFCAB surgery and blood samples were taken during and up to 24 h after the operation. We measured complement factors C5a and the terminal complement complex (TCC, C59-b), and the interleukins IL-6 and IL-8. Leukocytes were studied for cellular counts and adhesion molecules (CD11b, CD35 and CD62L) by flow cytometry. We included a combination of activity markers with different aspects of neutrophil function and combined these with in vitro activation. RESULTS: The complement factors C5a and TCC showed a more rapid (P=0.02, P<0.001) and TCC a more profound (P<0.001) increase in the ONCAB group than in the OFFCAB group during the operation, after that there were no inter-group differences. Cellular markers, cell counts and interleukin levels were activated by surgery but with no difference between groups. CONCLUSION: This prospective, randomised study showed less complement activation in low risk OFFCAB, compared to ONCAB patients.

Aged↗