scholarly journals Involvement of Antilipoarabinomannan Antibodies in Classical Complement Activation in Tuberculosis

1998 ◽  
Vol 5 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Geir Hetland ◽  
Harald G. Wiker ◽  
Kolbjørn Høgåsen ◽  
Beston Hamasur ◽  
Stefan B. Svenson ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complement Activation ◽  
Mononuclear Phagocytes ◽  
Factor B ◽  
Tuberculosis Patients ◽  
Terminal Complement Complex ◽  
Classical Activation ◽  
Normal Human ◽  
Terminal Complement ◽  
Classical Complement

ABSTRACT We examined alternative and classical complement activation induced by whole bacilli of Mycobacterium bovis BCG andMycobacterium tuberculosis products. After exposure to BCG, there were higher levels of the terminal complement complex in sera from Indian tuberculosis patients than in sera from healthy controls. The addition of BCG with or without EGTA to these sera indicated that approximately 70 to 85% of the total levels of the terminal complement complex was formed by classical activation. Sera from Indian tuberculosis patients contained more antibody to lipoarabinomannan (LAM) than sera from healthy Indians. Levels of anti-LAM immunoglobulin G2 (IgG2), but not anti-LAM IgM, correlated positively with classical activation induced by BCG in the sera. By flow cytometry, deposition of C3 and terminal complement complex on bacilli incubated with normal human serum was demonstrated. The anticomplement staining was significantly reduced in the presence of EGTA and EDTA. Flow cytometry also revealed the binding of complement to BCG incubated with rabbit anti-LAM and then with factor B-depleted serum. This indicates that classical activation plays a major role in complement activation induced by mycobacteria and that anti-LAM IgG on the bacilli can mediate this response. Classical complement activation may be important for the extent of phagocytosis of M. tuberculosis by mononuclear phagocytes, which may influence the course after infection.

scholarly journals FORMATION OF A HEMOLYTICALLY ACTIVE CELLULAR INTERMEDIATE BY THE INTERACTION BETWEEN PROPERDIN FACTORS B AND D AND THE ACTIVATED THIRD COMPONENT OF COMPLEMENT

1973 ◽  
Vol 138 (6) ◽  
pp. 1305-1313 ◽  
Author(s):  
Douglas T. Fearon ◽  
K. Frank Austen ◽  
Shaun Ruddy
Keyword(s):  
Complement System ◽  
Probable Mechanism ◽  
Factor B ◽  
Molecular Sequence ◽  
First Order ◽  
First Order Kinetics ◽  
The One ◽  
Terminal Complement ◽  
Classical Complement ◽  
Third Component Of Complement

The present studies demonstrate that the factor B-dependent C3 convertase can be affixed to an erythrocyte by use of an intermediate bearing C3b and that this convertase brings the hemolytic reaction to completion with an efficiency comparable to that of classical convertase. The evidence that the EAC43 intermediate was lysed by a new pathway includes requirements for factors B and D and cell-bound C3b for subsequent lysis by the terminal components, C3-C9. The linear stoichiometry of the effective molecule titrations of C3b and factor B, and the first-order kinetics displayed by the generation and decay of the factor B-dependent hemolytic site are characteristics consistent with the one-hit theory as initially developed for the classical complement system. The use of hemolytically active cellular intermediates to examine the reactions occurring with C3b and factors B and D has allowed extension of the one-hit theory to this molecular sequence, development of effective molecule titrations, recognition of the analogies to the functional characteristics of the classical C3 convertase, and discrimination of the probable mechanism of terminal complement activation from reactive lysis.

Flow cytometry based detection of HLA alloantibody mediated classical complement activation

2003 ◽  
Vol 275 (1-2) ◽  
pp. 149-160 ◽  
Author(s):  
Markus Wahrmann ◽  
Markus Exner ◽  
Heinz Regele ◽  
Kurt Derfler ◽  
Günther F. Körmöczi ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complement Activation ◽  
Classical Complement

Complement activation by cigarette smoke

1991 ◽  
Vol 260 (4) ◽  
pp. L254-L259 ◽  
Author(s):  
R. A. Robbins ◽  
K. J. Nelson ◽  
G. L. Gossman ◽  
S. Koyama ◽  
S. I. Rennard
Keyword(s):  
Human Serum ◽  
Cigarette Smoke ◽  
Complement Activation ◽  
Chemotactic Activity ◽  
Cigarette Smokers ◽  
Factor B ◽  
Alternate Complement Pathway ◽  
Normal Human ◽  
Properdin Factor B ◽  
The Complement System

Lung disease secondary to cigarette smoking is associated with an influx of neutrophils and monocytes into the lower respiratory tract. To determine whether cigarette smoke can generate chemotactic activity, human serum was exposed to cigarette smoke and evaluated for neutrophil and monocyte chemotactic activity. Serum exposed to cigarette smoke attracted significantly greater numbers of neutrophils and monocytes compared with normal human serum exposed to air (P less than 0.01, both comparisons). The increase in chemotactic activity was partially attenuated by EDTA but not by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and MgCl2 (P greater than 0.05, both comparisons), suggesting activation of the alternate complement pathway. To evaluate the capacity of cigarette smoke to activate the complement system, smoke-exposed serum was evaluated for cleavage of properdin factor B and C3 using immunoelectrophoresis and for C5a using a radioimmunoassay. Cleavage of properdin factor B and C3 was observed in the smoke-exposed serum and C5a was detected in the smoke-exposed serum (112 +/- 31 ng/ml). These data suggest that complement activation may play a role in directing the influx of neutrophils and monocytes into the lungs of cigarette smokers.

scholarly journals Complement activation in leprosy: a retrospective study shows elevated circulating terminal complement complex in reactional leprosy

2016 ◽  
Vol 184 (3) ◽  
pp. 338-346 ◽  
Author(s):  
N. Bahia El Idrissi ◽  
S. Hakobyan ◽  
V. Ramaglia ◽  
A. Geluk ◽  
B. Paul Morgan ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Complement Activation ◽  
Terminal Complement Complex ◽  
Terminal Complement

Complement activation in rheumatoid arthritis evaluated by C3dg and the terminal complement complex

1986 ◽  
Vol 29 (6) ◽  
pp. 715-721 ◽  
Author(s):  
Tom E. Mollnes ◽  
Tor Lea ◽  
Ove J. Mellbye ◽  
Jan Pahle ◽  
Øyvind Grand ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Complement Activation ◽  
Terminal Complement Complex ◽  
Terminal Complement

scholarly journals Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism

2019 ◽  
Vol 17 (6) ◽  
pp. 934-943 ◽  
Author(s):  
Ina I. Høiland ◽  
Robin A. Liang ◽  
Sigrid K. Brækkan ◽  
Kristin Pettersen ◽  
Judith K. Ludviksen ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Complement Activation ◽  
Terminal Complement Complex ◽  
Future Risk ◽  
Terminal Complement

scholarly journals Increase in the Complement Activation Product C4d and the Terminal Complement Complex sC5b-9 Is Associated with Disease Severity and a Fatal Outcome in Necrotizing Soft-Tissue Infection

2021 ◽  
pp. 1-11
Author(s):  
Morten Hedetoft ◽  
Martin Bruun Madsen ◽  
Cecilie Bo Hansen ◽  
Ole Hyldegaard ◽  
Peter Garred
Keyword(s):  
Soft Tissue ◽  
Disease Severity ◽  
Soft Tissue Infection ◽  
Complement Activation ◽  
Sofa Score ◽  
Tissue Infection ◽  
Necrotizing Soft Tissue Infection ◽  
High Baseline ◽  
Terminal Complement Complex ◽  
Terminal Complement

The hyperinflammatory burden is immense in necrotizing soft-tissue infection (NSTI). The complement system is a key during the innate immune response and may be a promising target to reduce the inflammatory response, potentially improving the clinical outcome. However, complement activation and its association to disease severity and survival remain unknown in NSTI. Therefore, we prospectively enrolled patients with NSTI and sampled blood at admission and once daily for the following 3 days. Plasma C4c, C4d, C3bc, and C3dg and the terminal complement complex (TCC) were evaluated using ELISA techniques. In total, 242 patients were included with a median age of 62 years, with a 60% male predominance. All-cause 30-day mortality was 17% (95% confidence interval [CI] 13–23) with a follow-up of &#x3e;98%. C4c and C3dg were negatively correlated with Simplified Acute Physiology Score II (<i>Rho</i> −0.22, <i>p</i> &#x3c; 0.001 and <i>Rho</i> −0.17, <i>p</i> = 0.01). Patients with septic shock (<i>n</i> = 114, 47%) had higher levels of baseline TCC than those in non-shock patients (18 vs. 14, <i>p</i> &#x3c; 0.001). TCC correlated with the Sequential Organ Failure Assessment (SOFA) score (<i>Rho</i> 0.19, <i>p</i> = 0.004). In multivariate Cox regression analysis (adjusted for age, sex, comorbidity, and SOFA score), high baseline C4d (&#x3e;20 ng/mL) and the combination of high C4d and TCC (&#x3e;31 arbitrary units/mL) were associated with increased 30-day mortality (hazard ratio [HR] 3.26, 95% CI 1.56–6.81 and HR 5.12, 95% CI 2.15–12.23, respectively). High levels of both C4d and TCC demonstrated a negative predictive value of 0.87. In conclusion, we found that in patients with NSTI, complement activation correlated with the severity of the disease. High baseline C4d and combination of high C4d and TCC are associated with increased 30-day mortality. Low baseline C4d or TCC indicates a higher probability of survival.

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