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PubMed1981

Interaction of the Legionnaires' disease bacterium (Legionella pneumophila) with human phagocytes. I. L. pneumophila resists killing by polymorphonuclear leukocytes, antibody, and complement.

We have previously reported that virulent egg yolk-grown Legionella pneumophila, Philadelphia 1 strain, multiplies intracellularly in human blood monocytes. We now report on the interaction between virulent L. pneumophila and human polymorphonuclear leukocytes (PMN), antibody, and complement, in vitro, under antibiotic-free conditions. L. pneumophila in concentrations ranging from 10(3) to 10(6) colony forming units (CFU)/ml are completely resistant to the bactericidal effects of 0-50 percent fresh normal human serum, even in the presence of high concentrations of rabbit or human anti-L. pneumophila antibody. L. pneumophila bacteria fix the third component of complement (C3) to their surfaces, as measured by fluorescence microscopy using rhodamine- conjugated goat anti-human C3 IgG, only when the bacteria are incubated with both specific anti-L. pneumophila antibody and complement. Similarly, L. pneumophila adhere to PMN, as measured by fluorescence microscopy, only in the presence of both specific antibody and complement. Electron microscopy revealed that these opsonized bacteria are phagocytosed by the PMN. PMN require both antibody and complement to kill L. pneumophila; even then, PMN reduced CFU of L. pneumophila by only 0.5 log under conditions in which they reduce CFU of a serum-resistant encapsulated strain of Escherichia coli by 2.5 logs. Separation of PMN-associated and nonassociated CFU of L. pneumophila revealed that the major proportion of the surviving bacteria are PMN associated. Thus, the ineffective killing of opsonized L. pneumophila is a result of a failure of PMN to kill these bacteria after they become PMN- associated. With or without antibody, PMN do not support the growth of L. pneumophila. These findings suggest that PMN, even in conjunction with the humoral immune system, do not play a decisive role in defense against the Legionnaires' disease bacterium.

Animals↗

PubMed1981

The pathology of mesangial IgA nephritis with clinical correlation.

Of 710 patients in whom renal biopsies with immunofluorescence, light and electron microscopic and clinical data were available, 239 had idiopathic mesangial IgA nephritis. In these 239 cases IgA was found alone in 45.7%, accompanied by IgG in 50.1%, IgM in 21.4%, C3 in 82.4% and fibrin in 37.2%. Serum immunoglobulin levels including IgA were not significantly raised and complement C3 activation was via the alternative pathway. There was a wide range of glomerular lesions with minor change, minor change with focal and segmental lesions including sclerosis and mesangial cell hypercellularity, diffuse mesangial cell proliferation and, infrequently, diffuse sclerosing glomerulonephritis. The glomerular leions were related to the stage, duration and severity of the disease. There was also a wide variability of clinical presentations, with asymptomatic and symptomatic microscopic haematuria-proteinuria, macroscopic haematuria, recurrent proteinuria, nephrotic syndrome, acute nephritis, hypertension, and uncommonly as acute renal failure and potassium losing nephritis. No aetiological agent was found, and both the streptococcus and HBsAg could not be identified. The disease(s) was the commonest type of primary glomerulonephritis (33.7%) in Singapore, another geographic area in addition to Japan and France, where this lesion has an apparent high incidence.

Adolescent↗

PubMed1976

Immunoglobulins attached to and in the integument of adult Schistosoma mansoni Sambon 1907, from first infection of CF mice.

7Sgamma2b antibody was found attached to and in the integument of adult Schistosoma mansoni removed from CF1 white mice. With the techniques used, IgA, IgM, 7Sgamma1, 7Sgamma2a, 7Sgamma3, and C3 complement were not found to be attached to the integumental surfaces. 7Sgamma2b does not seem to fix C3, and it is suggested this antibody may be acting in enhancing and blocking roles which protect the worms from the host.

Animals↗

PubMedDate not supplied

Role of fibronectin and complement in immunopathogenesis of acute and subacute hepatic failure.

The present study describes the plasma levels of soluble fibronectin (FN), C3d, the breakdown product of C3 complement and Ba, the breakdown product of properdin factor B, in 30 patients of uncomplicated acute viral hepatitis (AVH), 64 patients of fulminant hepatic failure (FHF) and 29 patients of subacute hepatic failure (SAHF) with different hepatitis viral infections. Aetiological analysis of these patients demonstrated hepatitis B, hepatitis C and hepatitis non-A, non-B, non-C (NANB-NC) infections in 6.7, 13.3 and 80% cases, respectively, of the AVH group; 18.8, 42.2. and 39.0% cases, respectively, of the FHF group; and 31.0, 34.5 and 34.5% cases of the SAHF group. None of them had hepatitis A infection. The analysis of data showed that the plasma FN level was significantly reduced in patients with FHF and SAHF as compared to AVH patients and healthy persons. Fibronectin levels in AVH was comparable to that in the healthy group. Further, the FN level was not dependent on the nature of aetiological virus. The level of C3d in plasma was significantly high in all patients of FHF and SAHF, irrespective of their viral aetiology, compared to the AVH group and the healthy group. Like FN, the C3d level was comparable in the AVH and healthy groups. However, the Ba level was comparable to the normal value in all types of infections including the AVH, FHF and SAHF groups. These findings were used to explain the possible roles of fibronectin and complement in the immunopathogenesis of liver injury in patients of acute liver failure of viral aetiology.

Adult↗

PubMed1999

Complement receptor type two (CR2,CR21): a target for influencing the humoral immune response and antigen-trapping.

Cellular receptors for complement C3 fragments deposited on antigens are important bricks in the wall defending against microbial pathogens. The part of complement receptor type 2 (CR2; CD21) deals with enhancing humoral immune responses and with long-term trapping of C3d-coated antigen by follicular dendritic cells. CR2 is also pivotal for Epstein-Barr virus (EBV) infection. Here, the current understanding, how CR2 interacts with its ligands C3d, EBV, and CD23 is summarized. The potential to target CR2 for clinical therapy or immunization purposes are discussed.

Adjuvants, Immunologic↗

PubMed2006

Opsonic requirements for the respiratory burst of neutrophils against Giardia lamblia trophozoites.

BACKGROUND: Giardia lamblia is an important cause of parasitic diarrheal disease worldwide. Occasionally, polymorphonuclear neutrophils (PMNs) may participate as effector cells against Giardia lamblia. The present study was performed in order to examine the role of specific antibody and complement components in promoting the respiratory burst (RB) of PMNs against Giardia lamblia. METHODS: PMNs from human adult volunteers were incubated with Giardia trophozoites in the presence of non-immune (NS) or hyperimmune (HS) serum (anti-Giardia titer, >1:1024). Adherence was scored visually on coverslide after staining with Giemsa. The ability of Giardia to trigger the oxidative response of PMNs was measured by the anion superoxide (O2(-)) production using a cytochrome C reduction method and by the luminol amplified chemiluminescence (CL) assay. RESULTS: Incubation with NS or HS increased Giardia adherence to PMNs from 6.9 +/- 3.2% (basal adherence of Giardia incubated in buffer) to 39 +/- 18.6% (p <0.01) and 76 +/- 19.5% (p <0.001), respectively. In absence of serum, Giardia failed to trigger an oxidative response of PMNs. Opsonization with NS or HS increased the PMN O2(-) production from 3.9 +/- 0.92 nmol/2.5 x 10(6) PMNs/10 min to 9.04 +/- 1.68 (p <0.05) and 17.9 +/- 1.32 (p <0.001), respectively. A similar enhancement of the CL response was also observed. The inactivation of complement activity by heat as well as the elimination of specific antibodies by absorption produced a significant abrogation of the oxidative response but in the case of HS heat inactivation alone did not abolish the response. Similar findings (variable abrogation of the oxidative PMN response) were observed when PMNs were incubated with monoclonal antibodies directed against complement C3, C3b or the low-affinity Fc receptors (CR1, CR3 or FcRlo). CONCLUSIONS: These results show that complement components and specific antibodies influence in the Giardia-PMN interaction. Although components of complement can contribute to the RB of PMNs, specific antibodies are critical for an optimal oxidative PMN response.

Animals↗

PubMedDate not supplied

Isolation of the third component of complement and its derivative with anaphylatoxin-like activity from the plasma of the newt Cynops pyrrhogaster.

The third component of complement (C3) of a newt, Cynops pyrrhogaster, was purified using a fast protein liquid chromatography technique. The purified newt C3 consists of two polypeptide chains (the molecular masses of the alpha and beta-chains of C3 were 120,000 and 70,000, respectively) linked by disulfide bonds. The alpha-chain retained an internal thiolester bond that was cleaved with methylamine, and the N-terminal amino acid sequence of the alpha-chain was XVQLIDAKAGKAAKF. Digestion of newt C3 with trypsin yielded fragments that induced significant histamine release from newt peritoneal cells. These results indicate that newt C3 retains structural and functional properties shared with mammalian C3.

Amino Acid Sequence↗

PubMed1983

Effect of maternal nutritional status on immunological substances in human colostrum and milk.

Substances in colostrum and breast milk confer significant disease resistance to the breast-fed infant. The influence of maternal nutritional status on both immunological and nonimmunological milk factors was studied in a group of 23 Colombian women during the first 2 months of lactation. Maternal malnutrition was characterized by significantly lower weight/height ratio, creatinine/height index, total serum proteins, serum albumin, and serum IgG and IgA. The colostrum of malnourished mothers contained only one-third the normal concentration of immunoglobulin G and less than half the normal level of albumin. Significant reductions in colostrum levels of IgA and the fourth component of complement (C4) were also observed in the malnourished group. No differences were observed in colostral concentrations of lysozyme, C3 complement, or IgM. Titers of antibody in milk directed against respiratory syncytial virus were not influenced by maternal nutritional status. The differences noted above tended to disappear in mature milk, concomitant with improvement in the nutritional status of malnourished mothers during the first several weeks postpartum. We conclude that the protective qualities of colostrum and milk may be significantly influenced by maternal nutritional status.

Adult↗

PubMed1988

A prospective study of acute idiopathic neuropathy. III. Immunological studies.

The immune responses of 100 patients who presented with an acute idiopathic neuropathy were compared with those of age and sex matched controls. Blood lymphocytes and their subsets were counted with a fluorescent activated cell sorter. CD8+ (putative suppressor) lymphocytes were significantly reduced in the first week of the disease but total lymphocytes, total T and CD4+ (putative helper) cells were not altered. This reduction depended on the nature of the preceding infection. Serum complement C3 and C4 concentrations remained normal and immune complexes were rarely detected with a C1q binding assay. Complement-fixing antibodies to human peripheral nerve antigens were discovered in the serum of 7% of patients but only 1% of controls. Complement-fixing antibodies to galactocerebroside were not discovered in any sera. Enzyme-linked immunoassays detected increased antibody responses to galactocerebroside but none at all to human P2 myelin protein in the patient sera. Forty microliter of serum from five patients injected into the sciatic nerves of rats did not induce significantly more demyelination than the serum from control patients. It is concluded that auto-immune responses can only be detected by these techniques in a small minority of patients with acute idiopathic neuropathy.

Adolescent↗

PubMed1998

Complement activation by diesel exhaust particles (DEP).

The effect of diesel exhaust particles (DEP) on the hemolytic activity of human serum complement was investigated. Previous treatment of human serum with DEP extracts at 37 degrees C decreased the hemolytic activity of human serum complement dose dependently, to 20% of its original value. This decrease in complement activity by DEP extracts was observed with previous incubation at 37 degrees C but not at 4 degrees C. A decrease in complement activity was observed after previous incubation at 37 degrees C in the presence of EGTA/Mg but not in the presence of EDTA, indicating that the alternative pathway of the complement system had been activated by DEP extracts. Activation of the complement system by DEP extracts was further demonstrated by observation of the cleavage of the third component of the complement (C3) in serum to C3b with immunoelectrophoresis using goat anti-human C3 antiserum. This cleavage of C3 was similarly observed in the presence of EGTA/Mg, indicating the activation of the alternative pathway of the complement system by DEP extracts. These results indicate that DEP can activate the alternative pathway of the complement system, resulting in a decrease in the hemolytic activity of complement and in the production of biologically active degradation products of complement proteins such as C3a. The biological significance of the activation of the complement by DEP in the alveolus is discussed in relation to the influx of neutrophiles.

Animals↗

PubMed2005

Anti-inflammatory effect of intravenous immunoglobulin mediated through modulation of complement activation.

Complement activation by immune complexes is well-known. In the course of autoimmune disease, acute and chronic complement activation is the primary inducer of inflammation and tissue damage. Polyclonal, polyspecific intravenous immunoglobulin (IVIg) preparations are a therapy of choice in a variety of autoimmune and inflammatory diseases. This review describes mechanisms by which IgG reduces complement activation or interferes with the action of proinflammatory complement-derived proteins. The known interference of IVIg with the biological activity of complement-derived proinflammatory proteins does not affect the generation of these potentially dangerous products, but can limit their devastating effects. Therefore, we embarked on studies on IVIg's potential to attenuate complement activation and thus to prevent further generation of such dangerous molecules. We present here a revised view of how the central event of complement activation--namely, complement amplification--operates on a molecular level and how IVIg, with its physiological autoantibodies directed against some complement proteins, is able to downregulate amplification of complement C3 activation. Finally, we summarize results of a study in which clinical effects of IVIg and attenuation of complement activation were assessed. We propose that the anti-inflammatory effect of IVIg in a wide range of autoimmune diseases might be explained, at least in part, by attenuation of complement amplification.

Animals↗

PubMed1993

Hereditary complete deficiency of the fourth component of complement: effects on the kidney.

Hereditary complete C4 deficiency has until now been detected in 18 patients. A disturbed clearance of immune complexes probably predisposes these individuals to systemic lupus erythematosus and other immune complex diseases. Renal involvement of hereditary complete C4 deficiency is described in seven patients from three families. Three patients of one family suffered from SLE and a severe mesangial and endocapillary proliferative glomerulonephritis which required immunosuppressive treatment. In two patients from a second family a mild focal and segmental mesangioproliferative glomerulonephritis was present which, except for an episode of acute renal failure in one patient, did not cause serious clinical problems. One additional child died without renal involvement. The patient from a third family developed Henoch-Schoenlein purpura, mesangioproliferative glomerulonephritis with segmental scarring and terminal renal failure. Immunofluorescence studies showed deposition of immunoglobulins and complement C3 in the glomeruli. Severity of renal disease is probably determined by activation of the alternative pathway of complement in the kidney.

Adolescent↗

PubMed1971

In vitro studies of complement function in sera of C4-deficient guinea pigs.

In vitro studies were performed utilizing sera from a strain of guinea pigs with a total absence of hemolytically active C4. Previous studies in these animals have demonstrated normal complement-dependent inflammatory reactions, suggesting that they are able to bypass their deficiency of C4. In vitro studies with C4-deficient serum also indicate normal activation of late-acting C components. Thus, endotoxin was capable of fixing normal amounts of the late components of complement (C3-9) in these sera, but did not fix C1 and C2. Antigen-antibody complexes fixed both early and late components of complement, although components beyond C4 were fixed less efficiently than in normal sera. Therefore, both in vivo and in vitro evidence indicates that the C4-deficient guinea pigs possess an alternate pathway for activation of late-acting complement components. Antigenic analysis of C4-deficient serum utilizing both guinea pig anti-C4 antibody and rabbit anti-C4 antibody suggests an absolute deficiency of C4-like molecules. Sera from animals with C4-deficiency were found to have one-half the normal level of C2. Sera from five of eight animals tested had 10-20% normal C1 activity. C3-9 assayed as a complex was normal.

Animals↗

PubMed2005

Activated human PMN synthesize and release a strongly fucosylated glycoform of alpha1-acid glycoprotein, which is transiently deposited in human myocardial infarction.

Alpha1-acid glycoprotein (AGP) is a major acute-phase protein present in human plasma as well as in polymorphonuclear leukocytes (PMN). In this report, we show that PMN synthesize a specific glycoform of AGP, which is stored in the specific and azurophilic granules. Activation of PMN results in the rapid release of soluble AGP. PMN AGP exhibits a substantially higher apparent molecular weight than plasma AGP (50-60 kD vs. 40-43 kD), owing to the presence of strongly fucosylated and sialylated polylactosamine units on its five N-linked glycans. PMN AGP is also released in vivo from activated PMN, as appeared from studies using well-characterized myocard slices of patients that had died within 2 weeks after an acute myocardial infarction. AGP was found deposited transiently on damaged cardiomyocytes in areas with infiltrating PMN only. It is interesting that this was inversely related to the deposition of activated complement C3. Strongly fucosylated and sialylated AGP glycoforms have the ability to bind to E-selectin and to inhibit complement activation. We suggest that AGP glycoforms in PMN provide an endogenous feedback-inhibitory response to excessive inflammation.

Complement Activation↗

PubMed2000

[The correlation between anticardiolipin antibodies and disease activity in patients with systemic lupus erythematosus].

This study was conducted to determine the prevalence and clinical association of anticardiolipin antibodies (ACA) in serum of patients with systemic lupus erythematosus (SLE). ACA (IgG, IgA, IgM) was measured by enzyme-linked immunosorbent assay (ELISA) in the serum sample of 87 patients of SLE. The prevalence rates of ACAIgG, ACAIgA and ACAIgM were 62.1%, 52.9% and 35.6% respectively. The titers of ACAIgG and ACAIgM were positively correlated with the disease activity (r = 0.2763, P = 0.044; r = 0.3294, P = 0.018); ACAIgG, ACAIgA and ACAIgM were negatively correlated with complement C3 (r = -0.4737, P = 0.000; r = -0.2990, P = 0.017; r = -0.2758, P = 0.029); and ACAIgG was negatively correlated with complement C4 (r = -0.4079, P = 0.005). The titers of ACAIgA in patients with thrombosis was higher than that in patients without thrombosis. The patients with central nervous system involvement (CNS-SLE) had significantly higher ACAIgG and ACAIgM titers, compared with those without CNS-SLE. The results indicate there is a correlation between ACA titers and disease activity. In patients with thrombosis, the titer of ACAIgA is higher, and in patients with CNS-SLE, the titers of ACAIgG and ACAIgM are higher.

Adolescent↗

PubMed1995

Early fulminant graft failure in orthotopic liver transplantation with massive haemorrhagic necrosis.

Early fulminant liver allograft failure is a post-transplant syndrome presenting as massive haemorrhagic necrosis of the graft. A single organ Shwartzman reaction has previously been suggested as a cause. We report on a patient who lost her liver graft due to fulminant graft failure ten days after orthotopic liver transplantation (OLT), the liver showing massive haemorrhagic necrosis. Fresh thrombosis was noted in the portal and hepatic veins. As a Shwartzman reaction could be expected to lead to complement deposition in vessel walls, tissue was analyzed for the presence of complement components. However, even though protein-rich and fibrinogen-containing deposits were detected within the vessel walls, these deposits were not immunoreactive for complement (C3 and Clq). These findings suggest that pathogenesis of fulminant liver allograft failure differs from that of a complement-mediated Shwartzman reaction, or of a hyperacute rejection, where IgM and Clq had previously been detected in hepatic veins and arteries.

Adult↗

PubMed1997

The comorbid association of migraine with osteoarthritis and hypertension: complement C3F and Berkson's bias.

Migraine is known to have a major genetic component and has been associated with a wide variety of comorbid disorders including arthritis and heart disease. Since migraine and some of its comorbid disorders involve inflammation, complement C3, a protein involved in acute inflammation, was selected for analysis as a candidate gene in an ongoing study of the genetic basis of migraine. Polymorphism frequencies for complement C3F (0.19) and C3S (0.81) in a sample of 137 unrelated migraineurs were found to be consistent with a control group as well as previous population studies, indicating that this common polymorphism has no association with migraine susceptibility. However, C3F positive individuals with migraine were found to have an increased incidence of osteoarthritis (Chi square = 10.06; p < 0.0008) and hypertension (Chi square = 5.18; p < 0.01). Therefore, the data in the present study indicate that certain migraine comorbidities that have been reported in the literature may result from Berkson's bias as opposed to a shared pathophysiological variation in the C3 gene.

Comorbidity↗

PubMed1990

Association of a 38 kDa bovine serum protein with the outer membrane of Bordetella pertussis.

Upon cultivation of Bordetella pertussis in bovine serum, a 38 kDa protein was found to be tightly associated with the outer membrane. The intensity of the 40 kDa porin was reduced under these growth conditions. Exposure of Bordetella pertussis, grown in Stainer and Scholte medium, to bovine serum for 1 h did not result in the appearance of the 38 kDa protein. Unlike the 40 kDa porin however, the electrophoretic mobility of this protein was affected neither by temperature of denaturation nor by the presence of 2-mercaptoethanol. Amino acid sequence analysis of the N-terminal of the 38 kDa protein revealed that his protein had 87% homology to both the mouse and human complement C3 precursors.

Amino Acid Sequence↗