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PubMed2003

[Study of immune response in Warao children from communities with high tuberculosis prevalence].

The present study was carried out in a Warao childhood population with extremely high tuberculosis (TB) rate of 3190/100,000 in 0-15 years old children. One hundred seven serum and saliva samples were tested, 32 from patients with active TB (27 positive and 5 negative for the tuberculin skin test, TST) and 75 apparently healthy contact children (45 positive and 30 negative for the TST). The innate, immunoglobulin and cellular responses were studied. The results showed that both, patients and controls, had a high percentage of children with increased levels of complement C3 and C4 components. A high percentage of children with increased total serum IgA and IgG (13.8% and 79.3% respectively) was observed in children with TB in comparison to control children (0% and 69.2%). A high percentage of control children had increased levels of IgM and sIgA (69.2% and 56.16%, respectively) in comparison to patients (48.3% and 31.25%). Both groups showed children with increased levels of IgE. The results concerning to the cellular immune response to PPD and the BCG vaccination status showed that there was a correlation between an increase in PPD reactivity and age. The PPD reactivity in children less than 7 years old was similar and also independent of the BCG vaccination status. A significant number of children without or with scars (46.8% and 27.6%, respectively) showed induration values of 0 mm to tuberculin skin test. The Candida reactivity showed a high percentage of children (80%) with anergy status. In conclusion, an increase in the levels of complement components C3 and C4 and hypergammaglobulinemia was observed in Warao children, and these results were independent from PPD reactivity and BCG vaccination. The isotype results showed that the decrease in sIgA could be and active disease marker, while the increase in IgM levels could represent a marker of recent disease.

Adolescent↗

PubMed1975

The influence of genotype on the development of glomerular lesions in mink with Aleutian disease virus.

In an attempt to document progression rate differences in the development of glomerular lesions in mink infected with Aleutian disease virus (ADV), the glomeruli of Aleutian and non-Aleutian mink experimentally infected with ADV were evaluated by light, fluorescent, and electron microscopy. The animals were also examined for the presence of interstitial infiltrate, neutrophils, and arterial lesions. One hundred percent of the Aleutian mink had glomerular cell proliferation and interstitial infiltrate, while 95% of the Aleutian and 41% of the non-Aleutian mink had neutrophilic infiltrates and arteritis, respectively. Of the non-Aleutian mink, 91, 83, 42, and 12.5% had glomerular cell proliferations, glomerular neutrophils, interstitial infiltrate, and arterial lesions in, that order. All the Aleutian mink had glomerular depositions of gamma-globulin (IgG) and complement (C3), whereas 75% of non-Aleutian mink had deposits of IgG and C3. One hundred percent of both genotypes had glomerular deposits of immunoglobulin M (IgM). Ultrastructural glomerular changes consisting primarily of depositions of granular electron-dense material on basement membranes were observed in Aleutian mink 6 weeks after infection and 12 weeks after infection in non-Aleutian mink. These findings document progression rate differences in the development of glomerular lesions in Aleutian disease-affected Aleutian and non-Aleutian mink. Further, they emphasize the need for exploration of pathogenetic mechanisms involved in progression rate differences in lesion development.

Aleutian Mink Disease↗

PubMed2003

Elastase-producing Pseudomonas aeruginosa degrade plasma proteins and extracellular products of human skin and fibroblasts, and inhibit fibroblast growth.

Leg ulcers of venous origin represent a disease affecting 0.1-0.2% of the population. It is known that almost all chronic ulcers are colonized by different bacteria, such as staphylococci, enterococci and Pseudomonas aeruginosa. We here report that P. aeruginosa, expressing the major metalloproteinase elastase, induces degradation of complement C3, various antiproteinases, kininogens, fibroblast proteins, and proteoglycans (PG) in vitro, thus mimicking proteolytic activity previously identified in chronic ulcer fluid in vivo. Elastase-producing P. aeruginosa isolates were shown to significantly degrade human wound fluid as well as human skin proteins ex vivo. Elastase-containing conditioned P. aeruginosa medium and purified elastase inhibited fibroblast cell growth. These effects, in conjunction with the finding that proteinase production was detected in wound fluid ex vivo, suggest that bacterial proteinases play a pathogenic role in chronic ulcers.

Apoptosis↗

PubMed1988

The effects of radiotherapy on the immune system of patients with nasopharyngeal carcinoma.

We report on 123 patients with nasopharyngeal carcinoma whose immune status was measured at the time of diagnosis, the day radiotherapy was completed, and then 2-3 months and 6-8 months after completion of radiotherapy. Immunological tests performed included the lymphocyte transformation test, the erythrocyte-rosette formation test (ERFT), the 29 degrees C erythrocyte-rosette formation test (29 degrees C ERFT), lymphocyte counts (lymphocytes/mm3 and percentage of lymphocytes), levels of serum immunoglobulins (IgG, IgA, IgM), complement (C3) and circulating immune complexes (CIC), the antinuclear antibody test and a skin test using phytohaemagglutinin (PHA). There were statistically significant differences in all tests (except C3) between patients and normal controls. Marked differences were seen in the lymphocyte count, ERFT, and 29 degrees C ERFT after radiotherapy (p less than 0.01). The diameters of induration of the PHA skin tests were less than those before radiotherapy (p less than 0.01). There were higher incidences of recurrence and metastases in the patients with high levels of CIC and low numbers of lymphocytes in the peripheral blood after radiotherapy. Cellular immunity remained at a low level 8 months after radiotherapy.

Antibodies, Antinuclear↗

PubMed1982

Isolation and analysis of genomic DNA clones encoding the third component of mouse complement.

A gene library was constructed with DNA from strain A mice by using the phage lambda vector lambda 1059. By screening with cloned cDNA for the third component of mouse complement, C3, four different C3 genomic clones were isolated from this library. Two of the recombinant phages carry insertions of 14 and 18 kilobase pairs, respectively, which together cover one complete copy of the C3 gene and several hundred nucleotides of its 5' and 3' flanking sequences. The distance from the 5' end of the gene, which includes the hexanucleotide T-A-T-A-A-A and a translation initiation codon, to its 3' end as defined by the poly(A) attachment site is 24 kilobase pairs. From the genomic DNA sequence, a signal peptide of 24 amino acid residues is predicted at the NH2 terminus of the initial translation product. The signal peptide and the next two amino acids are encoded by the first exon of this gene.

Animals↗

PubMed2004

Simultaneous analysis of host and pathogen interactions during an in vivo infection reveals local induction of host acute phase response proteins, a novel bacterial stress response, and evidence of a host-imposed metal ion limited environment.

A fundamental goal in the study of infections is to understand the dynamic interplay between host and pathogen; however, direct in vivo interrogation of this disease process via transcriptional profiling has been lacking. Here we describe the development and application of novel bacterial RNA amplification technology to simultaneously identify key elements of both host and pathogen responses in a murine infection model. On the bacterial side, we found induction of an unusual pattern of stress response genes, a response to host-induced metal ion limitation, and a failure to achieve stationary phase in vivo. On the mammalian side, we observed the surprising induction of several genes encoding acute phase response proteins including hepcidin, haptoglobin, complement C3 and metallothionein 1 at the site of infection, as well as other mediators of innate immunity. Thus, our results reveal host-pathogen cross-talk not predicted by previous in vitro analyses and provide the framework to eavesdrop on a broad array of host-pathogen interactions in vivo. As described here, the comprehensive examination of host-pathogen interactions during an infection is critical to the discovery of novel approaches for intervention not predicted by current models.

Acute-Phase Proteins↗

PubMed1990

Immunologic factors related to survival and performance in neonatal swine.

Logistic regression was used to develop models predicting preweaning survival in 334 neonatal swine. Measured risk factors included birth weight, litter size (live born), dam parity, serum IgG concentration, serum ELISA titers recognizing common gram-negative core antigens, and serum concentrations of the third component of complement. Larger birth weights were associated with increased probability of preweaning survival. The highest mortality was observed in litters with more than 12 pigs. Pigs with serum concentration of the third component of complement (C3) in the lowest stratum, less than 20% adult pooled C3 standard (APC3), had reduced mortality, compared with high (greater than 38% APC3) and middle (20 to 38% APC3) groups. Associations between all other variables, including total serum IgG concentration and preweaning survival were not significant. Few pigs had hypogammaglobulinemia, less than 3% of the study population had serum IgG concentrations less than 1 g/dl. Of all measured variables, only birth weight and dam parity were significant predictors of preweaning gain. Larger pigs and pigs born to third or greater parity dams had more preweaning gain than other pigs.

Animals↗

PubMed1997

A comparison of the suppression of human transferrin synthesis by lead and lipopolysaccharide.

Transferrin, as the major iron-transport protein in serum and other body fluids, has a central role in managing iron the body receives. Liver is a major site of transferrin synthesis, and in this study we present evidence that liver synthesis of human transferrin is suppressed by both the toxic metal lead and bacterial lipopolysaccharide, an inducer of the hepatic acute phase response. The responses of intact endogenous transferrin in the human hepatoma cell line HepG2 and chimeric human transferrin-chloramphenicol acetyltransferase genes in transgenic mice were examined. In HepG2 cells, 35S-transferrin protein synthesis and mRNA levels were suppressed by 100 microM and 10 microM lead acetate as early as 24 h after the initial treatment. Yet, synthesis of two proteins known to respond in the hepatic acute phase reaction, complement C3 and albumin, was not altered by the lead treatment. In transgenic mouse liver, lead suppressed expression of chimeric human transferrin genes at both the protein and mRNA levels, but LPS only suppressed at the protein level. The study indicates that lead suppresses human transferrin synthesis by a mechanism that differs from the hepatic acute phase response and that lead may also affect iron metabolism in humans by interfering with transferrin levels.

Acute-Phase Reaction↗

PubMed2002

Genetic-biochemical criteria for individual sensitivity in development of occupational bronchopulmonary diseases.

Human individual sensitivity to health-hazardous occupational factors and probability of developing chronic lung diseases depend on genetic variation of serum and erythrocytic proteins. The present work was aimed at studying the phenotypes of serum and erythrocytic proteins in patients with occupational respiratory diseases. We studied 7 highly polymorphic genetic systems the varieties of which may be connected with development of bronchopulmonary pathology (BPP) and the immune status of the body: proteinase inhibitor (Pi), third component of the complement (C3), transferrin (Tf), group-specific component of blood serum (Gc), haptoglobin (Hp), erythrocytic glyoxalase (Glo) and phosphoglucomutase (PGM) in patients with chronic bronchitis, silicosis, occupational bronchial asthma and in the control group consisting of Moscow population not exposed to occupational hazards and apparently healthy workers of an engineering plant. Considerable differences were revealed in genetic structure of the patients with bronchopulmonary pathology as compared with the apparently healthy people along a series of Integrated system: proteinase inhibitor (Pi), C3, Tf, Gc, PGM. Comparison of the study groups by significant differences in the aggregate of the genetic information obtained suggests that 5 (HP, C3, Tf, Pl, PGM1) of the 7 studied systems showed the hereditary features of silicosis. The gene carriers Hp*2, C3*F, PGM1*2-, TF*D, GC*R due to peculiar biochemical processes appear to have less adaptive potentialities and a greater likelihood of the disease on exposure to industrial factors. The examined patients with chronic bronchitis showed an increase in the variant of GC*2 and of a rare variants of proteins GC*R and Pi*S, the patients with occupational bronchial asthma showed an increase in the variant of Hp*2 and of a rare variant Pi*S. Such studies could be useful for assessment and forecast of individual risk of occupational diseases.

Alleles↗

PubMed2004

Poststreptococcal glomerulonephritis with pulmonary edema presenting as respiratory distress.

Acute poststreptococcal glomerulonephritis(PSGN) is characterized by an abrupt onset of edema,hypertension, and hematuria. Although the association of pulmonary edema with acute glomerulonephritis has been established, it is uncommon for children with PSGN to present with respiratory distress due to pulmonary edema. We encountered six such patients, aged 6-10 years, during a 10-month period. The demographic data, clinical manifestations, laboratory data, radiographic pictures, and clinical courses were collected. All patients presented to the primary pediatricians with dyspnea and alveolar infiltrates with bilateral pleural effusions on plain chest radiographs that were misinterpreted as pneumonia initially. The diagnosis of PSGN was de-layed until the awareness of the presence of pulmonary edema complicating PSGN. Subsequent urinalysis and blood pressure measurement all showed microscopic hematuria and hypertension. Elevated serum antistreptolysin 0 titers and depressed serum complement C3 levels confirmed the diagnosis of PSGN. Two patients progressed to respiratory failure because of a delayed diagnosis of PSGN. All patients recovered without sequelae following appropriate diuresis and antihypertensive therapy. We conclude that in preschool and school-age children who present with dyspneic respirations and a chest radiograph showing radiographic features of pulmonary edema, proper evaluation including blood pressure recording and urinalysis should be performed immediately. Prompt diagnosis and early therapy of PSGNmay avoid mortality and unnecessary therapeutic intervention.

Anti-Bacterial Agents↗

PubMed1999

Proteolytic destruction of functional proteins by phagocytes in human peritonitis.

BACKGROUND: Besides phagocyte-derived oxidative autoaggression, proteolytic destruction of functional proteins in the peritoneal cavity may also be involved in the pathomechanism of secondary peritonitis. To evaluate the pattern of proteolysis, 43 patients undergoing initial operation for acute peritonitis (n = 30) or scheduled abdominal lavages (Etappenlavage) for resolution of persistent peritonitis (n = 13) and 16 surgical patients with abdominal exudation without peritonitis were enrolled in our study. MATERIALS AND METHODS: Thirty blood samples and purulent exudates were taken simultaneously in each peritonitis group at the surgical interventions. Sixteen clear exudates were obtained from patients with post-operative non-infectious irritations. The following parameters were measured: (a) elastase (from neutrophils) and cathepsin B (from monocytes/macrophages); (b) alpha1-proteinase inhibitor (alpha1PI) and overall cysteine proteinase inhibitor capacity; and (c) opsonic activity and degradation products of fibrinogen, complement C3 and immunoglobulin IgG. RESULTS: Circulating levels of phagocyte proteinases and of alpha1PI were significantly elevated, whereas antigen concentrations and opsonic activity of C3 and IgG were slightly reduced in peritonitis patients compared to healthy volunteers. No degradation products were detectable in patients' blood. Discharge of phagocyte proteinases was even more pronounced in both types of peritonitis exudates. Although most of the elastase was complexed with alpha1PI, active elastase and its specific fibrinogen split product was found along with significantly reduced inhibitory capacity for elastase and cysteine proteinases. Local opsonic activity was dramatically diminished because of proteolytic degradation of C3 and IgG. Despite some phagocyte proteinase release, no destruction of functional proteins was seen in clear exudates. CONCLUSIONS: Higher values of extracellularly released phagocyte proteinases concomitant with lower opsonin activity in exudates from patients with persistent peritonitis can be taken as a further hint of the involvement of local proteolysis-induced pathomechanisms in the development of lethal multiple organ failure, which occurred more frequently in patients with persistent peritonitis (54%) than in those with acute peritonitis (27%).

Adolescent↗

PubMed1988

Immunoglobulins and complement in demyelination induced in mice by Theiler's virus.

Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) produces chronic demyelination and persistent infection in the central nervous system (CNS) of susceptible SJL mice. This series of experiments examined the contribution of humoral immunity and C to myelin destruction. As in multiple sclerosis, mice persistently infected with TMEV had elevated levels of IgG and oligoclonal bands in the cerebrospinal fluid (CSF). Immunoblot studies revealed that even in animals exhibiting profound demyelination, IgG in the serum and CSF was directed primarily at virus antigen rather than at normal myelin components. Inflammatory cells positive for Ig were distributed mainly around blood vessels, but occasionally they infiltrated the spinal cord parenchyma. Rare examples of myelin sheaths positive for IgG were found by immunoelectron microscopy in spinal cord sections from infected mice; the third component of complement (C3) was commonly found in the walls of CNS blood vessels but not on myelin. Neither serum nor CSF IgG from infected mice bound to myelin sheaths or other CNS components in sections of normal syngeneic spinal cord. There were significantly more demyelinating lesions in infected mice depleted of C components with cobra venom factor. These data do not support a humoral autoimmune basis for the CNS demyelination that occurs in association with persistent TMEV infection. However, the humoral immune response directed at TMEV antigens may either limit virus spread or promote virus persistence.

Animals↗

PubMed1993

Immunofluorescent analysis of extracellular matrix (ECM) components in glomeruli of the hepatic glomerulosclerosis.

An immunofluorescence study was carried out to evaluate alterations in the distribution and/or intensity of extracellular matrix (ECM) components, immunoglobulins and complement (C3) in the glomeruli of 7 autopsy patients with hepatic glomerulosclerosis. As compared with the findings in normal renal tissues, an increase in type IV collagen, laminin and fibronectin was observed in expanded glomerular mesangial areas and along glomerular capillary walls. Depositions of IgA, mainly IgA1, and C3 in glomeruli were in parallel with those of the ECM components. These ECM components were markedly decreased in glomeruli showing global sclerosis. In contrast, type I collagen was observed at central portions of the sclerotic glomeruli. There was an increase in the type I collagen along Bowman's capsules, especially at the sites of capsular adhesion and crescent formation. It appears that hyperproduction and/or infiltration of glomerular ECM components and interstitial collagen is closely linked to the progression of glomerular sclerosis in patients with liver diseases.

Adult↗

PubMed1998

Early phagocytosis of glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes parasitized by Plasmodium falciparum may explain malaria protection in G6PD deficiency.

In population-based studies it has been established that inherited deficiency of erythrocyte (E) glucose-6-phosphate dehydrogenase (G6PD) confers protection against severe Plasmodium falciparum (P falciparum) malaria. Impaired growth of parasites in G6PD-deficient E in vitro has been reported in some studies, but not in others. In a systematic analysis, we have found that with five different strains of P falciparum (FCR-3, KI, C10, HB3B, and T9/96), there was no significant difference in either invasion or maturation when the parasites were grown in either normal or G6PD-deficient (Mediterranean variant) E. With all of these strains and at different maturation stages, we were unable to detect any difference in the amount of P falciparum-specific G6PD mRNA in normal versus deficient parasitized E. The rate of 14C-CO2 production from D-[1-14C] glucose (which closely reflects intracellular activity of G6PD) contributed by the parasite was very similar in intact normal and deficient E. By contrast, in studies of phagocytosis of parasitized E by human adherent monocytes, we found that when the parasites were at the ring stage (ring-stage parasitized E [RPE]), deficient RPE were phagocytosed 2.3 times more intensely than normal RPE (P = .001), whereas there was no difference when the parasites were at the more mature trophozoite stage (trophozoite-stage parasitized E [TPE]). Phagocytic removal markers (autologous IgG and complement C3 fragments) were significantly higher in deficient RPE than in normal RPE, while they were very similar in normal and deficient TPE. The level of reduced glutathione was remarkably lower in deficient RPE compared with normal RPE. We conclude that impaired antioxidant defense in deficient RPE may be responsible for membrane damage followed by phagocytosis. Because RPE, unlike TPE, are nontoxic to phagocytes, the increased removal by phagocytosis of RPE would reduce maturation to TPE and to schizonts and may be a highly efficient mechanism of malaria resistance in deficient subjects.

Animals↗

PubMed1990

[An immunologic study of patients with epilepsy].

Eight indices of the immunological function were studied in 246 adult epileptic patients with 100 normal adults as control, it was found that mean contents of blood IgA, and IgM decreased, that of complement C3 increased, and the rates of lymphocyte transformation as well as rosette formation decreased in this group of epileptic patients. The decrease of IgA was related to the types of seizures and the taking of antiepileptic drugs. Suggesting that immunological abnormality did exist in the epileptic patients. The mean content of circulating immune complexes. (CIC) had a negative correlation with the period of time after seizures. It was much higher than that of the controls within the first 3 days after the seizures with its highest levels reached on the first day. Suggesting that immune reactions took part in the process of seizure episodes.

Adolescent↗

PubMed1985

Antispermatozoal antibodies in human follicular fluid.

The possibility of antispermatozoal antibodies in women having significant effects in the higher regions of the female reproductive tract has been investigated. Follicular fluids (FF) and sera taken at the time of oocyte recovery from women undergoing in vitro fertilisation and embryo transfer (IVF-ET) were tested for the presence of antispermatozoal antibodies, and the concentrations of IgM, IgG, IgA, and complement C3 were determined. The concentrations of immunoglobulins and C3 in FF were consistent with transudation from serum inversely proportional to molecular weight. Titres of agglutinating and immobilizing antibodies in FF were usually one or two dilution steps below those of serum except where immobilizing activity was associated with IgM. IgG:IgA ratios were lower in FF from women with antispermatozoal antibodies, suggesting local production or enhanced transudation of IgA; however, a secretory component could not be detected in any of the follicular fluids in this study. Two women with antispermatozoal antibodies and infertility in excess of 5 years had successful IVF-ET and have delivered healthy infants.

Antibody Specificity↗

PubMed2003

A strategy for the comparative analysis of serum proteomes for the discovery of biomarkers for hepatocellular carcinoma.

Many of the emerging technologies for the global evaluation of gene expression, at both the RNA and protein level, are being applied to the problem of finding biomarkers for human disease progression. These analyses can be made difficult, however, by variation between samples that arises from both technical and nondisease related physiological or genetic causes. In an effort to identify serum polypeptides whose presence or absence correlates with the clinical status of patients at high risk for hepatocellular carcinoma (HCC), we have developed a strategy that helps to focus the analysis on meaningful changes in protein levels above the background of variation. For the current study we divided the patient population into four clinically defined diagnostic groups that represent a generally increasing risk for HCC. Chronic infection with hepatitis B virus (HBV) is a major risk factor for HCC and our groups included patients with no indication of liver disease (healthy), those with inactive chronic HBV, those with active chronic HBV, and patients with a diagnosis of HCC and history of chronic HBV infection. Serum polypeptides from these patients were first analyzed in two-dimensional gels by combining the serum from patients in each of the four groups to generate composite gel profiles. Analysis of these composite gels allowed us to identify two relatively abundant features that were reduced in the HCC group as compared to the healthy group. Tryptic fragment mass fingerprinting identified the features as a carboxy terminal fragment of complement C3 and an isoform of apolipoprotein A1. These two features were examined by two-dimensional gel electrophoresis of serum from each individual in the four groups in order to verify that the inter-group differences seen in composite gels reported changes in abundance for most members of the group, rather than extreme changes for a small fraction of the group. These preliminary studies suggest that a proteomic methodology can be used for the identification of serum biomarkers for HCC and other liver disease.

Amino Acid Sequence↗

PubMed1984

Genetic markers in carcinoma of the prostate.

The distribution of phenotypes and gene frequencies of the third component of complement (C3), group-specific component (Gc), haptoglobin (Hp) and transferrin (Tf) were studied in 115 patients with carcinoma of the prostate. The statistical analysis of our findings in comparison to the frequency of these genes in a control group of 155 patients with benign prostatic hyperplasia does not reveal any correlation between the distribution of the Hp and Tf phenotypes and the disease. On the contrary, a statistically significant association was found between carcinoma of prostate and C3F and Gc2 genes. The relative risk incidence of this malignancy is 1.56 and 1.81, respectively, for the carriers of these genes suffering from benign prostate hyperplasia.

Complement C3↗