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At least 775 records · Page 43Linked to original sources
PubMed1985

Murine natural resistance to Trypanosoma lewisi involves complement component C3 and radiation-resistant, silica dust-sensitive effector cells.

The phenomenon of natural (innate) resistance is exemplified by the solid resistance of mice to infection with the rat-specific Trypanosoma lewisi. We provide more information about the mechanism of resistance in this model system. Resistance was not diminished in aged mice or reduced by ionizing radiation or splenectomy. There was no difference in resistance of C5-deficient mice (B10.D2/oSn and AKR) compared with their normocomplementemic counterparts (B10.D2/nSn and C57BL/6). Treatment of mice with cobra venom factor resulted in greatly prolonged survival of T. lewisi in mice. Combined treatment of mice with cobra venom factor and silica dust resulted in not only prolonged survival but also considerable intravascular growth of the parasite and resultant death of the mice. T. lewisi cells from irradiated donor rats, or after surface coat removal with trypsin, were eliminated by inoculated mice more efficiently than were parasites acquired from normal rats. Incubation of trypanosomes obtained from irradiated rats in normal rat serum restored their resistance to rapid elimination. From the results of these studies and other recent investigations, we have concluded that murine resistance to T. lewisi involves activation and binding of C3b by uncoated trypanosomes and concomitant participation of radiation-resistant, silica dust-sensitive effector cells (probably macrophages and neutrophils), and rat plasma proteins, integrated into the trypanosome surface coat, stabilize the coat, make it less susceptible to removal when the trypanosome is present in the mouse bloodstream, and thus delay exposure of underlying molecules (receptors?) that activate murine C3.

Animals↗
PubMed1999

Neurological manifestations of chronic hepatitis C.

Hepatitis C virus (HCV) infection is often associated with abnormal immunological responses. We describe four patients with vasculitic neurological signs and symptoms following HCV infection. A 56-year-old woman with HCV infection developed peripheral neuropathy characterized by asymmetric distal painful hypesthesia, dysesthesia and moderate motor weakness of the lower limbs. Serological examinations revealed cryoglobulinemia and low levels of complement C4. A biopsy of the sural nerve revealed vasculitic neuropathy. HCV infection associated immunomediated vasculitis was diagnosed. While steroid therapy was ineffective, treatment with interferon-alpha improved the neuropathy considerably without, however, eliminating HCV infection. A 62-year-old man with HCV infection developed peripheral sensory neuropathy. Complement C3 was slightly diminished. Nerve biopsy revealed vasculitic neuropathy. A 71-year-old woman developed chronic symmetric sensomotor polyneuropathy. HCV hepatitis followed blood transfusions. Cryoglobulins tested positive, consistent with type II cryoglobulinemia. Complements C3 and C4 were diminished. Inflammatory infiltrates in the sural nerve biopsy specimen led to the diagnosis of chronic vasculitic disorder. A 55-year-old woman with HCV infection developed vasculitis of the skin, connective tissue, visceral organs, and kidney, leading to hemodialysis. Neurologically she developed severe apathy and drowsiness, myoclonic jerks, exaggerated deep tendon reflexes, and positive pyramidal signs. Magnetic resonance imaging of the brain showed diffuse increased signal abnormalities involving supra- and infratentorial white matter suggesting cerebral vasculitis. Cryoglobulins were positive, complements C3 and C4 slightly diminished (54 mg/dl, 4.3 mg/dl). Supportive therapy resulted in neurological improvement. Treatment with interferon-alpha was discontinued because of agranulocytosis. In patients with peripheral neuropathy or signs of leucencephalopathy, a hepatitis C associated vasculitis should be considered in the differential diagnosis.

Aged↗
PubMed1989

[Partial lipodystrophy and membranoproliferative glomerulonephritis. Apropos of a case].

We have studied a girl seven and a half years old with a renal disease manifested by proteinuria and nephrotic syndrome combined with initial macroscopic hematuria normal blood pressure and persistent depression of the complement C3 levels with the complement activating gamma globulin (C3 Nef) present in serum. The anatomopathological study showed findings of membranoproliferative glomerulonephritis type II with intramembranous deposit (dense deposit disease). An unusual association with partial lipodystrophy was present in this case. A follow-up of five years, and a few considerations about etiopathogenic theories were presented.

Child↗
PubMed1995

Extracellular matrix induces hormone responsiveness and differentiation in RUCA-I rat endometrial adenocarcinoma cells.

We recently described the establishment and the characterization of two rat endometrial adenocarcinoma cell lines which we called RUCA-I and RUCA-II. Despite fairly high estrogen receptor levels neither cell line responded to estradiol in conventional cell culture conditions on plastic and in the presence of serum. A limited hormonal response to the antiestrogen tamoxifen was detectable in RUCA-I but not in RUCA-II cells. To advance our cell culture conditions we plated RUCA-I cells on a layer of reconstituted basement membrane (Harbor Matrix) in the presence of a serum-free defined medium. These cell culture conditions induced hormone responsiveness of RUCA-I cells and permitted a stimulation of proliferation by estradiol. Further, two estradiol-induced secretory proteins with an apparent molecular weight of 115 kD and 60 kD could be identified by SDS-gelelectrophoresis if analyzed under reducing conditions. These proteins migrated as a single band in a non-reducing electrophoresis gel and were identified as components of the complement C3 system. Additionally, our results suggest that the effects of extracellular matrix and hormones on the expression of these proteins are additive. We conclude that processes of functional differentiation are most likely to occur in this in vitro model, particularly since the expression of components of the complement C3 system was under estrogenic control. Complement C3 proteins represent major estradiol-inducible secretory protein of the immature rat uterus in vivo. Culturing RUCA-I cells on top of a layer of reconstituted basement membrane provides a novel tool to study the importance of the extracellular environment on the hormone-induced gene expression in endometrial carcinogenesis in vitro.

Adenocarcinoma↗
PubMed2004

The ontogeny of complement component C3 in Atlantic cod (Gadus morhua L.)--an immunohistochemical study.

The complement system in fish is well developed and plays an important role in the immune response. Very little is known about the ontogeny of C3 in fish and no study has previously been done on the development of C3 in teleosts. In this study we have detected the presence of C3 in cod larvae from the age of 1 day post hatching (p.h.) till 57 days p.h., using immunohistochemistry. The specific primary antibodies used, were produced against the beta-chain of cod C3. Immunostaining on cod larvae sections revealed that C3 is detectable in the yolksac membrane from day 1 p.h., and in liver, brain, kidney and muscle from day 2 p.h. C3 was also detected in other organs such as eye, notochord, stomach, intestines, pancreas, heart and gills at different stages of cod larval development. These findings suggest that complement is not only important in immune defence against invading pathogens but may also play a role in the formation and generation of different organs.

Animals↗
PubMed2004

Pentoxifylline inhibits tumor necrosis factor-alpha induced synthesis of complement component C3 in human endothelial cells.

Vascular endothelium is a major target for the inflammatory damage that occurs with multiple organ dysfunction associated with sepsis and other trauma. The growing appreciation of endothelium as a target of inflammation has obscured the importance of these cells as a source of inflammatory mediators. In the following study we evaluated the ability of tumor necrosis factor-alpha (TNF) to induce the synthesis of complement component C3 in human umbilical vein endothelial cells (HUVEC) and whether pentoxifylline (PTX) could reduce C3 expression. Confluent monolayers of HUVEC were treated with increasing concentrations of TNF with and without two concentrations of PTX. Concentrations of C3 were determined every 48 h for 144 h in cellular supernatants and C3 mRNA was amplified using RT-PCR. TNF increased C3 release from HUVEC in a concentration dependent manner. PTX added at the same time as TNF significantly reduced C3 release at the 96 h time point. Consistent with data on C3 release PTX inhibited the increased C3 mRNA expression associated with TNF treatment. TNF increases C3 synthesis and release from endothelial cells which were inhibited by clinical concentrations of PTX. This data further supports the potential benefit of PTX in multiple organ dysfunction and other inflammatory processes involving the endothelium by inhibiting one of the major mediators of vascular damage.

Cells, Cultured↗
PubMed1994

Appearance of immunoglobulin G and complement factor C3 in the striatum after transient focal ischemia in the rat.

The pathophysiological feature of brain ischemia-infarct was investigated using immunohistochemistry and Gallyas' silver staining after transient ischemia of the middle cerebral artery (MCA) in the rat. A very strong IgG infiltration with clear-cut borders was detected at one to 3 days in ischemic core areas (lateral striatum and adjacent cortex) that fell into porencephaly later. Complement factor C3 (C3) immunoreactivity (IR) appeared similarly while albumin IR more diffusely. Microglial activation could be observed at 1 day while rounded leukocyte-like elements at 3 days after reperfusion. Data suggest that the early appearance of the IgG/C3 IR bears particular importance after transient MCA ischemia as it could predict the ensuing porencephaly in the chronic stage.

Albumins↗
PubMed1983

Complement-activating immune deposits in systemic lupus erythematosus skin.

Immune deposits at the cutaneous basement membrane zone are a characteristic feature of systemic lupus erythematosus. Previous studies using immunofluorescent methods to detect complement components have provided evidence that some deposits contain immune complexes capable of activating complement. However, this important biologic property of complexes has not been detected or measured using functional assays, and it has not been determined whether immune deposits can activate complement at the basement membrane zone. In this study immune deposits in biopsies of lupus skin have been examined using direct immunofluorescence for the third component of complement (C3) to detect complement deposited in vivo. In addition, the deposits have been studied using the leukocyte attachment assay and indirect C3 binding immunofluorescence to detect and measure complement activation at the basement membrane zone in vitro. The results show that complement activation occurs at the basement membrane in some but not all lupus skin containing immunoglobulin deposits, that deposits differ quantitatively in their ability to activate complement, and that direct C3 immunofluorescence is a relatively insensitive method for detecting complement-activating complexes. The results provide functional evidence suggesting that immune deposits in some lupus skin are complement-activating complexes and potentially capable of activating complement at the basement membrane in vivo. Furthermore, the results suggest functional assays for evaluating complement-activating complexes may be valuable supplements to immunofluorescence in exploring the relationship between immune deposits and systemic and cutaneous disease.

Basement Membrane↗
PubMed1989

Determination of amino acid compositions and NH2-terminal sequences of peptides electroblotted onto PVDF membranes from tricine-sodium dodecyl sulfate-polyacrylamide gel electrophoresis: application to peptide mapping of human complement component C3.

The combination of high-resolution Tricine-Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (H. Schägger and G. von Jagow (1987) Anal. Biochem. 166, 368-379) and electroblotting onto polyvinylidene difluoride (PVDF) membranes represents a powerful technique for the isolation of small amounts of peptides and protein fragments (Mr 1000-20,000) in a suitable form for amino acid sequencing, directly on the blotting membrane. Conditions for electrophoresis and electroblotting were optimized with respect to high transfer yield and suitability for both amino acid analysis and sequence determination of stained PVDF-bound peptides. Transfer yields were 50-80%, amino acid compositions including Cys were correct, and picomole quantities were sequenced with initial and repetitive yields as high as those we normally obtain for peptides in solution. The method was used for peptide mapping of polymorphic forms of human complement component C3.

Amino Acid Sequence↗