RESUMO
INTRODUCTION: Eosinophilic meningoencephalitis due to Angiostrongylus cantonensis is an emergent infectious disease in our area. The objective of the present paper is to determine if the activation of the complement system was taken placed with the C3c production in cerebrospinal fluid. PATIENTS AND METHODS: 14 patients with an average age 4.5 years were studied. In such patients a lumbar punction was performed. C3c was quantified in serum and cerebrospinal fluid by radial immunodiffusion. RESULTS: Median cell number was 396 x 10(-6)/L with an average of 8.8% of eosinophils. Main symptoms were headache, vomiting and fever. Meningeal signs were present in 50% of the patients. C3c intrathecal synthesis occurred in 13 patients (92.8%). CONCLUSION: It was demonstrated the participation of complement system in third-stage larvae destruction in cerebrospinal fluid.
Assuntos
Angiostrongylus cantonensis , Helmintíase do Sistema Nervoso Central/imunologia , Complemento C3/líquido cefalorraquidiano , Complemento C3/fisiologia , Eosinofilia/imunologia , Eosinofilia/parasitologia , Meningoencefalite/imunologia , Meningoencefalite/parasitologia , Infecções por Strongylida/imunologia , Animais , Pré-Escolar , Complemento C3/biossíntese , HumanosRESUMO
Since there are no studies evaluating the participation of the complement system (CS) in Jorge Lobo's disease and its activity on the fungus Lacazia loboi, we carried out the present investigation. Fungal cells with a viability index of 48% were obtained from the footpads of BALB/c mice and incubated with a pool of inactivated serum from patients with the mycosis or with sterile saline for 30 min at 37 masculineC. Next, the tubes were incubated for 2 h with a pool of noninactivated AB+ serum, inactivated serum, serum diluted in EGTA-MgCl2, and serum diluted in EDTA. The viability of L. loboi was evaluated and the fungal suspension was cytocentrifuged. The slides were submitted to immunofluorescence staining using human anti-C3 antibody. The results revealed that 98% of the fungi activated the CS by the alternative pathway and no significant difference in L. loboi viability was observed after CS activation. In parallel, frozen histological sections from 11 patients were analyzed regarding the presence of C3 and IgG by immunofluorescence staining. C3 and IgG deposits were observed in the fungal wall of 100% and 91% of the lesions evaluated, respectively. The results suggest that the CS and immunoglobulins may contribute to the defense mechanisms of the host against L. loboi.
Assuntos
Ativação do Complemento/fisiologia , Proteínas do Sistema Complemento/fisiologia , Imunoglobulinas/imunologia , Paracoccidioides/fisiologia , Animais , Ativação do Complemento/imunologia , Complemento C3/imunologia , Complemento C3/fisiologia , Proteínas do Sistema Complemento/imunologia , Imunofluorescência , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Paracoccidioides/imunologiaRESUMO
Complement-depleted and -non-depleted BALB/c mice were inoculated with Leishmania (Leishmania) amazonensis promastigotes into the hind footpad to study the role of the complement system in cutaneous leishmaniasis. Total serum complement activity was measured by hemolytic assay and C3 fragment deposit at the inoculation site was determined by direct immunofluorescence in the early period of infection, i.e., at 3, 24, 48 h and 7 days post-infection. The inflammatory reaction and the parasite burden were evaluated in the skin lesion at 7 and 30 days post-infection. Total serum complement activity decreased in the early phase of infection, from 3 to 24 h, in non-depleted mice compared to non-infected and non-depleted mice. C3 fragment deposit at the site of parasite inoculation was present throughout the period of infection in non-depleted mice. In contrast, no C3 fragment deposit was observed at the inoculation site in complement-depleted mice. Complement-depleted mice showed a significant decrease in the inflammatory response and a significant increase in the number of parasites (70.0 +/- 5.3 vs 5.3 +/- 1.5) at 7 days of infection (P<0.05). A higher number of parasites were also present at 30 days of infection at the inoculation site of complement-depleted mice (78.5 +/- 24.9 vs 6.3 +/- 5.7). These experiments indicate that complement has an important role at the beginning of experimental cutaneous leishmaniasis caused by L. (L.) amazonensis by controlling the number of parasites in the lesion.
Assuntos
Proteínas do Sistema Complemento/fisiologia , Leishmania , Leishmaniose Cutânea/imunologia , Animais , Ativação do Complemento , Complemento C3/fisiologia , Ensaio de Atividade Hemolítica de Complemento , Leishmaniose Cutânea/parasitologia , Depleção Linfocítica , Masculino , Camundongos , Camundongos Endogâmicos BALB CRESUMO
We have assessed the potential involvement of C(3), the third complement factor, and its receptor in Bufo arenarum fertilization. We show that a polyclonal antibody against a B. arenarum C(3)-like factor (C(3)Ba) reacts specifically with components of the extracellular matrix (ECM) of coelomic eggs and the cell membrane of uterine eggs. Interestingly, we have identified a 163 kD protein immunoreactive with a monoclonal antibody against the CD11b alpha chain of the human C(3) receptor on the cell membrane of the animal pole of uterine eggs, the site of entry of the sperm, but not in coelomic eggs (CR3Ba). Treatment of coelomic eggs with a pars recta oviductal-like protease, trypsin, induced the translocation of C(3)Ba from the ECM to the cell membrane. Furthermore, inhibition of CR3Ba by trypan blue, as well as inhibition of C(3)Ba by anti-C(3)Ba on uterine eggs impaired fertilization, whereas identical treatment on sperm cells did not alter percentage fertilization. Our results suggest, (A) that changes in the localization of C(3)Ba from the ECM to the cell membrane may be triggered by trypsin-like proteases during passage of eggs through the oviduct; and (B) that C(3)Ba/CR3Ba may be involved in B. arenarum fertilization.
Assuntos
Bufo arenarum/fisiologia , Complemento C3/fisiologia , Fertilização , Animais , Anticorpos/metabolismo , Anticorpos/farmacologia , Especificidade de Anticorpos , Complemento C3/antagonistas & inibidores , Feminino , Fertilização in vitro , Imunofluorescência , Masculino , Óvulo/metabolismo , Receptores de Complemento/metabolismo , Espermatozoides/metabolismoRESUMO
PROBLEM: To determine whether any blood plasma factor may play a regulatory role in trophoblast phagocytosis in rodent early pregnancy. METHOD OF STUDY: The effects of alloplasma on the phagocytosis of cultured mouse trophoblast cells (TCs) were evaluated using erythrocytes as target cells, in the presence of 10% fresh, normal plasma; 10% heat-inactivated plasma; 10% component 3 (C3)-depleted plasma; or medium alone. The possible activation of C3 complement, the phagocytosis of zymosan bound or unbound to C3b, and immunoreactivity to C3b receptor were also estimated. Phagocytic activity was expressed as the percentage of phagocytic TCs, and as the number of phagosomes/TCs. RESULTS: The use of complement sufficient plasma significantly enhanced the phagocytosis of the TCs while the use of heat-inactivated plasma eliminated the erythrophagocytosis. Very low levels of phagocytic activity were seen when the plasma was C3-complement deficient. Phagocytosis of C3b-bound zymosan was remarkable in comparison to zymosan alone, and immunoreactivity to C3b-receptors was seen on the TCs. CONCLUSION: These results indicate the participation of thermosensitive molecules mediating the phagocytosis of TCs and suggest, as in macrophages, a role for C3-C3b in this process.
Assuntos
Ativação do Complemento , Complemento C3/fisiologia , Fagocitose , Trofoblastos/imunologia , Animais , Feminino , Imuno-Histoquímica , Masculino , Camundongos , Camundongos Endogâmicos AKR , Gravidez , Zimosan/metabolismoRESUMO
Cutaneous lesions induced by infection of mice with the protozoan parasite, Leishmania mexicana, contain abundant amounts of a high molecular mass proteophosphoglycan (PPG), which is secreted by the amastigote stage residing in phagolysosomes of macrophages and can then be released into the tissue upon rupture of the infected cells. Amastigote PPG forms sausage-shaped but soluble particles and belongs to a novel class of serine-rich proteins that are extensively O-glycosylated by phosphooligosaccharides capped by mannooligosaccharides. The purified molecule is shown here to efficiently activate complement (C) and deplete hemolytic activity of normal serum and may prevent the opsonization of L. mexicana amastigotes. Complement activation is Ca2+ dependent but does not depend on antibodies or the complement component C1. PPG binds to serum mannan binding protein (MBP), thus activating the MBP-associated serine protease, P100. Subsequently, the C cascade is triggered through C4 leading to covalent modification probably of carbohydrate hydroxyls of PPG by C3 fragments. Thus, PPG is able to activate C via the mannan binding lectin pathway which is unusual for secreted, soluble products of microbial origin. The proteophosphoglycan-induced complement activation is postulated to contribute to the lesion development and pathology caused by the parasite.
Assuntos
Proteínas de Transporte/fisiologia , Ativação do Complemento/efeitos dos fármacos , Leishmania mexicana/fisiologia , Leishmaniose Cutânea/imunologia , Proteoglicanas/fisiologia , Proteínas de Protozoários/fisiologia , Animais , Cálcio/fisiologia , Colectinas , Complemento C3/fisiologia , Complemento C4/fisiologia , Macrófagos/parasitologia , Camundongos , Camundongos Endogâmicos CBA , Camundongos Knockout , Proteoglicanas/isolamento & purificação , Proteoglicanas/farmacologia , Proteínas de Protozoários/isolamento & purificação , Proteínas de Protozoários/farmacologiaRESUMO
1. Trypanosoma cruzi epimastigote forms are very rapidly removed from the circulation of normal and C5-deficient mice. Depletion of C3 by cobra venom factor results in a significant delay in parasite clearance. 2. During parasite clearance there is a significant decrease in the number of circulating platelets and parasite clearance is considerably delayed in thrombocytopenic animals. 3. In vitro incubation of epimastigote forms with normal mouse serum leads to the formation of parasite clumps provided that platelets are present. Inactivation of factor B or depletion of C3 prevents this phenomenon. 4. When epimastigotes are incubated with normal mouse serum they absorb one or more factors required for their aggregation with platelets. 5. It is suggested that in mice T. cruzi epimastigote forms are removed from circulation by the alternative pathway of complement activation and that both C3 and platelets are required for parasite clearance.
Assuntos
Plaquetas/fisiologia , Complemento C3/fisiologia , Complemento C5/fisiologia , Trypanosoma cruzi/fisiologia , Animais , Ativação do Complemento , Camundongos , Camundongos Endogâmicos A , Camundongos Endogâmicos BALB C , Agregação PlaquetáriaRESUMO
1. The role of IgG antibody and platelets in the mechanism of defense against Trypanosoma cruzi infection is reviewed. 2. Experimental data showing the participation of the different IgG subclasses in the immune lysis and immune clearance of the parasites are discussed. 3. The involvement of the platelets in the removal of the parasites from the circulation is considered. 4. It is suggested that IgG anti-T. cruzi antibodies interact with circulating parasites leading to formation of microaggregates, activation of C3 and deposition of C3b on the immune aggregates followed by adherence of platelets through C3b receptors. The immune aggregates would then be taken up by cells of the mononuclear phagocytic system.
Assuntos
Anticorpos Antiprotozoários/fisiologia , Plaquetas/fisiologia , Doença de Chagas/imunologia , Imunoglobulina G/fisiologia , Animais , Ativação do Complemento , Complemento C3/fisiologia , Complemento C3b/fisiologia , Humanos , Imunização , CamundongosRESUMO
1. The role of IgG antibody and platelets in the mechanism of defense against Trypanosoma cruzi infection is reviewed. 2. Experimental data showing the participation of the different IgG subclasses in the immune lysis and immune clearance of the parasites are discussed. 3. The involvement of the platelets in the removal of the parasites from the circulation is considered. 4. It is suggested that IgG anti-T. cruzi antibodies interact with circulating parasites leading to formation of microaggregates, activation of C3 and deposition of C3 and deposition of C3b on the immune aggregates followed by adherence of platelets through C3b receptors. The immune aggregates would then be taken up by cells of the mononuclear phagocytic system
Assuntos
Humanos , Animais , Camundongos , Anticorpos Anti-Idiotípicos/fisiologia , Plaquetas/fisiologia , Doença de Chagas/imunologia , Imunoglobulina G/imunologia , Ativação do Complemento , Complemento C3b/fisiologia , Complemento C3/fisiologia , ImunizaçãoRESUMO
This review outlines: a) the main biochemical and biological properties of the complement system (C) components; b) the manner through which they interact in the two distinct routes of C activation, the classical and the alternative pathways, to generate the enzymes C3 and C5 convertases responsible for release of the peptides C4a, C3a and C5a endowed with the properties of mediating the early events of the inflammatory process or the potentially cytolytic complex C5b-C9; c) the main features of control of these activation processes; d) the identification of cell surface components present in the trypomastigote forms of Trypanosoma cruzi possibly involved in the mechanisms developed by this parasite to evade C lysis; e) the inactivation or removal of these cell surface components by enzymatic (trypsin or papain), chemical (periodate) or physical (heating at 45 degrees C) treatments; f) isolation of these components by chromatographic methods; and, g) demonstration that some of these cell surface components interfere with C3 convertase formation or action in a manner similar to the decay accelerating factor (DAF).