The activation of the complement system by Paracoccidioides brasiliensis in vitro: Its opsonic effect and possible significance for an in vivo model of infection

1979 ◽  
Vol 12 (1) ◽  
pp. 20-30 ◽  
Author(s):  
Vera L.G. Calich ◽  
Thereza L. Kipnis ◽  
M. Mariano ◽  
C.Fava Neto ◽  
W.Dias da Silva
Keyword(s):  
Complement System ◽  
Paracoccidioides Brasiliensis ◽  
In Vivo Model ◽  
The Complement System

scholarly journals Anti-GD2 IgA kills tumors by neutrophils without antibody-associated pain in the preclinical treatment of high-risk neuroblastoma

2021 ◽  
Vol 9 (10) ◽  
pp. e003163
Author(s):  
Mitchell Evers ◽  
Marjolein Stip ◽  
Kaylee Keller ◽  
Hanneke Willemen ◽  
Maaike Nederend ◽  
...  
Keyword(s):  
High Risk ◽  
Sensory Neurons ◽  
Complement System ◽  
Severe Pain ◽  
Neuroblastoma Cells ◽  
Antibody Therapy ◽  
Preclinical Treatment ◽  
The Complement System

BackgroundThe addition of monoclonal antibody therapy against GD2 to the treatment of high-risk neuroblastoma led to improved responses in patients. Nevertheless, administration of GD2 antibodies against neuroblastoma is associated with therapy-limiting neuropathic pain. This severe pain is evoked at least partially through complement activation on GD2-expressing sensory neurons.MethodsTo reduce pain while maintaining antitumor activity, we have reformatted the approved GD2 antibody ch14.18 into the IgA1 isotype. This novel reformatted IgA is unable to activate the complement system but efficiently activates leukocytes through the FcαRI (CD89).ResultsIgA GD2 did not activate the complement system in vitro nor induced pain in mice. Importantly, neutrophil-mediated killing of neuroblastoma cells is enhanced with IgA in comparison to IgG, resulting in efficient tumoricidal capacity of the antibody in vitro and in vivo.ConclusionsOur results indicate that employing IgA GD2 as a novel isotype has two major benefits: it halts antibody-induced excruciating pain and improves neutrophil-mediated lysis of neuroblastoma. Thus, we postulate that patients with high-risk neuroblastoma would strongly benefit from IgA GD2 therapy.

The Interaction of Liposomes with the Complement System: In Vitro and In Vivo Assays

2003 ◽  
pp. 136-154 ◽  
Author(s):  
Janos Szebeni ◽  
Lajos Baranyi ◽  
Sandor Savay ◽  
Janos Milosevits ◽  
Michael Bodo ◽  
...  
Keyword(s):  
Complement System ◽  
In Vivo Assays ◽  
The Complement System

Introduction to the complement system

1984 ◽  
Vol 306 (1129) ◽  
pp. 279-281 ◽  
Keyword(s):  
Humoral Immunity ◽  
Complement System ◽  
Bacterial Infections ◽  
Cross Linking ◽  
Complement Components ◽  
The Third ◽  
Effector Mechanism ◽  
The Complement System

Complement is the essential effector mechanism in humoral immunity to infection. Combination of antibody with antigen causes cross-linking, leading to precipitation of soluble antigens and agglutination of particular antigens, but no more. Unless complement is also present, agglutinated microorganisms can, in appropriate media in vitro grow out and form as lethal a culture as if not reacted with antibody. That this is also true in vivo is apparent from experience with patients with inherited deficiencies in complement components. The pattern is complex because of the presence of two pathways of activation, but in the rare cases of deficiency of the third component, C3, which is central to both pathways, the individuals are susceptible to repeated bacterial infections similar to aggammaglobulinaemics who are unable to synthesize antibodies. Both antibodies and complement are essential for effective humoral immunity.

The Role of Membrane Bound Complement in the Aggregation of Mammalian Platelets by Collagen

1975 ◽  
Author(s):  
B. V. Chater
Keyword(s):  
Electron Microscope ◽  
Light Microscopy ◽  
Complement System ◽  
Membrane Bound ◽  
The Complement System ◽  
Adhesion Of Platelets ◽  
Collagen Stimulation

It has been observed in dogs decomplemented with purified Cobra Venom Factor, that their platelets lose the ability to aggregate in response to collagen stimulation. Further investigation of the effect of CVF in vitro in man, dog and rabbit, and in vivo in dog, reveals that in each case CVF abolishes the collagen response of platelets, and that this effect is dose related. Resuspension of CVF inactivated platelets in plasma containing complement, results in a total return of sensitivity to collagen. Examination of CVF inactivated platelets with the electron microscope, fails to show any marked difference from control platelets. Serotonin granules are still present and the platelets retain a discoid appearance. Incubation of platelets with antibodies to Cl, C3 and C5, results in inhibition of the collagen response, this effect also being dose related. Light microscopy studies indicate that CVF does not affect the adhesion of platelets to collagen but appears to prevent subsequent aggregation. It is suggested that the complement system is involved in the induction of release by collagen, and that inhibition by CVF and anti-complement antibodies is the result of a blocking of the release reaction.

Charge and Size Heterogeneity of C3d following in vivo and in vitro Activation of the Complement System

Complement ◽  
1984 ◽  
Vol 1 (1) ◽  
pp. 36-43 ◽  
Author(s):  
B. Teisner ◽  
J. Hau ◽  
J. Folkersen ◽  
H.H. Jepsen
Keyword(s):  
Complement System ◽  
In Vitro Activation ◽  
Size Heterogeneity ◽  
The Complement System

scholarly journals Zonulin as prehaptoglobin2 regulates lung permeability and activates the complement system

2013 ◽  
Vol 304 (12) ◽  
pp. L863-L872 ◽  
Author(s):  
Daniel Rittirsch ◽  
Michael A. Flierl ◽  
Brian A. Nadeau ◽  
Danielle E. Day ◽  
Markus S. Huber-Lang ◽  
...  
Keyword(s):  
Complement System ◽  
Serine Proteases ◽  
Neutralizing Antibody ◽  
Dependent Manner ◽  
Neutrophil Accumulation ◽  
The Complement System ◽  
Dose Dependent

Zonulin is a protein involved in the regulation of tight junctions (TJ) in epithelial or endothelial cells. Zonulin is known to affect TJ in gut epithelial cells, but little is known about its influences in other organs. Prehaptoglobin2 has been identified as zonulin and is related to serine proteases (MASPs, C1qrs) that activate the complement system. The current study focused on the role of zonulin in development of acute lung injury (ALI) in C57BL/6 male mice following intrapulmonary deposition of IgG immune complexes. A zonulin antagonist (AT-1001) and a related peptide with permeability agonist activities (AT-1002) were employed and given intratracheally or intravenously. Also, zonulin was blocked in lung with a neutralizing antibody. In a dose-dependent manner, AT-1001 or zonulin neutralizing antibody attenuated the intensity of ALI (as quantitated by albumin leak, neutrophil accumulation, and proinflammatory cytokines). A similar pattern was found using the bacterial lipopolysaccharide model of ALI. Using confocal microscopy on sections of injured lungs, staining patterns for TJ proteins were discontinuous, reduced, and fragmented. As expected, the leak of blood products into the alveolar space confirmed the passage of 3 and 20 kDa dextran, and albumin. In contrast to AT-1001, application of the zonulin agonist AT-1002 intensified ALI. Zonulin both in vitro and in vivo induced generation of complement C3a and C5a. Collectively, these data suggest that zonulin facilitates development of ALI both by enhancing albumin leak and complement activation as well as increased buildup of neutrophils and cytokines during development of ALI.

scholarly journals Bothrops aspersnake venom and its metalloproteinase BaP–1 activate the complement system. Role in leucocyte recruitment

2000 ◽  
Vol 9 (5) ◽  
pp. 213-221 ◽  
Author(s):  
Sandra H. P. Farsky ◽  
Luís Roberto C. Gonçalves ◽  
José M. Gutiérrez ◽  
Adriana P. Correa ◽  
Alexandra Rucavado ◽  
...  
Keyword(s):  
Complement System ◽  
Neutrophil Migration ◽  
Neutrophil Chemotaxis ◽  
C5a Receptor ◽  
Haemolytic Assay ◽  
Leucocyte Recruitment ◽  
The Complement System ◽  
Deficient Mice

The venom of the snakeBothrops asper, the most important poisonous snake in Central America, evokes an inflammatory response, the mechanisms of which are not well characterized. The objectives of this study were to investigate whetherB. aspervenom and its purified toxins – phospholipases and metalloproteinase – activate the complement system and the contribution of the effect on leucocyte recruitment.In vitrochemotaxis assays were performed using Boyden's chamber model to investigate the ability of serum incubated with venom and its purified toxins to induce neutrophil migration. The complement consumption by the venom was evaluated using anin vitrohaemolytic assay. The importance of complement activation by the venom on neutrophil migration was investigatedin vivoby injecting the venom into the peritoneal cavity of C5-deficient mice. Data obtained demonstrated that serum incubated with crude venom and its purified metalloproteinase BaP–1 are able to induce rat neutrophil chemotaxis, probably mediated by agent(s) derived from the complement system. This hypothesis was corroborated by the capacity of the venom to activate this systemin vitro. The involvement of C5a in neutrophil chemotaxis induced by venom-activated serum was demonstrated by abolishing migration when neutrophils were pre-incubated with antirat C5a receptor antibody. The relevance of the complement system inin vivoleucocyte mobilization was further demonstrated by the drastic decrease of this response in C5-deficient mice. Pre-incubation of serum with the soluble human recombinant complement receptor type 1 (sCR 1) did not prevent the response induced by the venom, but abolished the migration evoked by metalloproteinase-activated serum. These data show the role of the complement system in bothropic envenomation and the participation of metalloproteinase in the effect. Also, they suggest that the venom may contain other component(s) which can cause direct activation of C5a.

Effect of salicylates on the complement system: Generation of mediators in vivo and in vitro

1981 ◽  
Vol 21 (2) ◽  
pp. 228-236 ◽  
Author(s):  
G.M. Hänsch ◽  
W. Römer ◽  
V. Voigtländer ◽  
U. Rother
Keyword(s):  
Complement System ◽  
System Generation ◽  
The Complement System
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