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PubMedDate not supplied

[Anemia in chronic renal insufficiency--case report].

INTRODUCTION: Chronic renal insufficiency is a clinical syndrome including increased urea in the serum and creatinine concentration with or without decrease of urine production. Numerous diseases may induce chronic renal insufficiency. In developed countries these are most often diabetes mellitus, glomerulonephritis and hypertension, whereas in developing countries these are bacterial infections, gall stone, tuberculosis and some parasitic diseases. Chronic renal insufficiency leads to functional disorders of all systems in the body, including hematopoiesis. Anemia is a common complication, while its degree depends on the degree of creatmemia. It is normocytic and normochromic. Anemia is caused by several factors, decreased erythropoietin synthesis being the most important. The stimulus for its secretion is tissue hypoxia. Erythropoietin synthesis is regulated by mechanism of negative retroaction and it stimulates proliferation. It also prevents apoptosis--programmed cell death. Other important factors causing anemia are uremic toxins, which decrease proliferation of erythroid progenitors, damage erythrocytes and shorten their life. Changes in the microvascular system of kidneys also cause anemia mechanically damaging erythrocytes and hemolysis. Patients with chronic renal insufficiency are susceptible to hemorrhages (erosions and duodenal ulcers) being one of the factors causing anemia. Recombinant erythropoietin production and its application in treatment of chronic renal insufficiency patients is of great importance. It is applied subcutaneously and intravenously, whereas the dosage and length of treatment are individual. CASE REPORT: A female patient, (M. R.) 69 years of age, has been treated at the Department of Internal Diseases of the Hospital in Senta 22 times during the last 30 years. Chronic renal insufficiency was caused by chronic pyelonephritis and hypertension. Up to two years ago she had several transfusions and received 7.480 ml of deplasmatic erythrocytes. The last transfusion was in May 1997, due to hemoglobin values lower than 80 g l. In August 1997, the patient acquired recombinant erythropoietin and was hospitalized and treated in our institution by subcutaneous application of erythropoietin (50 mu kg) every other day, with monitoring of hemoglobin, hematocrit, erythrocyte count increase and values of serum iron. The therapeutic response was good. 14 months later she was hospitalized again and the therapy was repeated. The last outpatient follow-up was on January 5, 1999, and hemoglobin was 92 g l. CONCLUSION: Our case report shows that recombinant erythropoietin gives good results in treatment of anemia: correction of anemia, improvement of general status and there is no need for frequent transfusions and thus there are less complications.

Aged↗

PubMed2005

Mechanism of D(2) agonist-induced inhibition of GH secretion from human GH-secreting adenoma cells.

The mechanism of dopamine D(2) agonist-induced inhibition of GH secretion from GH-secreting adenoma cells was investigated by measurement of intracellular calcium concentration ([Ca(2+)] (i)) and static incubation experiment. Bromocriptine decreased [Ca(2+)](i) in a concentration-dependent manner through D(2) receptor. The inhibition was abolished by pertussis toxin pretreatment. Bromocriptine did not decrease [Ca (2+)](i) after nitrendipine had decreased it. 8Br-cAMP increased [Ca(2+)](i) but application of bromocriptine decreased it, suggesting that bromocriptine-induced inhibition of [Ca(2+)](i) is not dependent on bromocriptine-induced inhibition of adenylyl cyclase. Static incubation experiment revealed that bromocriptine inhibited GH secretion in a concentration-dependent manner. The inhibition was through D(2) receptor and was abolished by pertussis toxin pretreatment. 8Br-cAMP increased GH secretion. Bromocriptine decreased GH secretion even after 8Br-cAMP pretreatment. However, the GH release from cells incubated with bromocriptine alone was significantly less than that from cells incubated with bromocriptine after 8Br-cAMP pretreatment, suggesting a modulatory action of cAMP system in bromocriptine response.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2000

Properties of cytotoxic peptide-formed ion channels.

Cytotoxic peptides are relatively small cationic molecules such as those found 1) in venoms, e.g., melittin in bee, scorpion toxins in scorpion, pilosulin 1 in jumper ant, and lycotoxin I and II in wolf spider; 2) in skin secretions (e.g., magainin I and II from Xenopus laevis, dermaseptin from frog, antimicrobials from carp) and cells of the immune system (e.g., insect, scorpion, and mammalian defensins and cryptdins); 3) as autocytotoxicity peptides, e.g., amylin cytotoxic to pancreatic beta-cells, prion peptide fragment 106-126 [PrP-(106-126)], and amyloid beta-protein (AbetaP) cytotoxic to neurons; and 4) as designed synthetic peptides based on the sequences and properties of naturally occurring cytotoxic peptides. The small cytotoxic peptides are composed of beta-sheets, e.g., mammalian defensins, AbetaP, amylin, and PrP-(106-126), whereas the larger cytotoxic peptides have several domains composed of both alpha-helices and beta-sheets stabilized by cysteine bonds, e.g., scorpion toxins, scorpion, and insect defensins. Electrophysiological and molecular biology techniques indicate that these structures modify cell membranes via 1) interaction with intrinsic ion transport proteins and/or 2) formation of ion channels. These two nonexclusive mechanisms of action lead to changes in second messenger systems that further augment the abnormal electrical activity and distortion of the signal transduction causing cell death.

Amino Acid Sequence↗

PubMed2001

Local and systemic immune responses to rectal administration of recombinant cholera toxin B subunit in humans.

The induction of immune responses to rectally administered recombinant cholera toxin B subunit (CTB) in humans was studied. Three immunizations induced high levels of CTB-specific antibody-secreting cells, particular of the immunoglobulin A isotype, in both rectum and peripheral blood. Antitoxin antibody responses in rectal secretions and serum were also found.

Administration, Rectal↗

PubMed1990

The small intestine: prospects for therapeutic approaches in secretory diarrhoeal diseases.

In many diarrhoeal diseases the intestinal mucosa is stimulated to secrete salt and water. This occurs in diarrhoea as a result of several bacterial toxins, is associated with inflammation and release of inflammatory mediators, and, in many instances, occurs when a neural element is evident. An understanding of the basic underlying mechanisms of secretion could lead to improvements in therapy. Development of vaccines against cholera is showing promise, and a knowledge of the complex field of inflammatory mediators, many of which provoke secretion, provides a foundation for development of more specific and selective anti-inflammatory agents. A detailed understanding of the complicated intracellular second-messenger systems, which are switched on by externally perceived signals, and of the ion transport responses, which are responsible for secretion, may lead to the development of specific anti-diarrhoeal drugs. Meanwhile, the message that oral rehydration therapy for severe diarrhoea, including cholera, is successful, should continue to be widely promulgated and taken up.

Acute-Phase Proteins↗

PubMed1994

The yeast killer phenomenon: a hypothetical way to control Pneumocystis carinii pneumonia.

Pneumocystis carinii is an important agent of pneumonia in immunocompromised individuals, especially in acquired immunodeficiency syndrome AIDS patients P. carinii attaches specifically to type 1 pneumocytes. Although this phenomenon must play a marked role in pneumocystosis pathophysiology, no therapeutic molecules able to inhibit specifically the parasite attachment were found. A killer toxin, secreted by the yeast Pichia anomala, induced a significant decrease in P. carinii in vitro attachment and inhibited the parasite infectivity in SCID mice. Killer toxins cannot be used as systemic antibiotics. However, it was possible to produce antiidiotypic antibodies against a monoclonal antibody specific of the toxin active site. These antilds were shown to mimic the in vitro killer effect for the toxin and were called 'antibiobodies'. The susceptibility of P. carinii to the antimicrobial activity of the killer toxin made it possible to hypothesize that the killer phenomenon could constitute a new way for the treatment and prophylaxis of P. carinii infections.

Animals↗

PubMed2001

The two-component system ArlS-ArlR is a regulator of virulence gene expression in Staphylococcus aureus.

Staphylococcus aureus is a major human pathogen that produces many virulence factors in a temporally regulated manner controlled by at least two global virulence regulatory loci (agr and sarA). We identified previously a two-component system, ArlS-ArlR, that modifies the activity of extracellular serine protease and may be involved in virulence regulation. Here, we show that mutations in either arlR or arlS increase the production of secreted proteins [alpha-toxin (Hla), beta-haemolysin, lipase, coagulase, serine protease (Ssp)] and especially protein A (Spa). Furthermore, the pattern of proteins secreted by both mutants was strikingly different from that of the wild-type strain. Transcriptional fusions showed that expression of hla, ssp and spa was higher in both mutants than in the wild-type strain, indicating that the arl operon decreases the production of virulence factors by downregulating the transcription of their genes. The arl mutation did not change spa expression in an agrA mutant or in a sarA mutant, suggesting that both the sarA and the agr loci are required for the action of arl on spa. Northern blot analyses indicated that the arl mutation increased the synthesis of both RNA II and RNA III, but decreased sarA transcription. Finally, arl was not autoregulated, but its expression was stimulated by agr and sarA. These results suggest that the Arl system interacts with both agr and sarA regulatory loci to modulate the virulence regulation network.

Bacterial Proteins↗

PubMed2006

Members of a Legionella pneumophila family of proteins with ExoU (phospholipase A) active sites are translocated to target cells.

Legionella pneumophila replicates within alveolar macrophages, causing a severe pneumonia termed Legionnaires' disease. The bacterium resides within a vacuole that escapes immediate transport to the host lysosome. Instead, the vacuole interacts with the early secretory pathway to establish an environment suitable for rapid multiplication. A type IV secretion system is central to the pathogenicity of the bacterium, and many protein substrates that are translocated by this system to the host cell have been identified. One of these, VipD, was found to interrupt the late secretory pathway when overproduced in Saccharomyces cerevisiae. We independently identified VipD in a previous study and have further characterized this protein as well as its three paralogs. The vipD gene belongs to a family of L. pneumophila open reading frames that are predicted to contain a phospholipase A domain with sequence similarity to the type III-secreted toxin ExoU from Pseudomonas aeruginosa. Similarly to other known translocated proteins of L. pneumophila, VipD is strongly induced in early stationary phase, a time when the bacterium is most virulent. Detergent extraction studies of infected macrophages confirm that VipD is translocated into host cells via the type IV secretion system. A second assay for translocation revealed that two paralogs of VipD, VpdA and VpdB, also have translocation signals recognized by the type IV system. A strain lacking VipD and its three paralogs grew at wild-type rates in murine macrophages, although secondary mutations that cause growth defects in strains lacking VipD accumulate. The quadruple mutant displayed a growth advantage in the amoebal host Dictyostelium discoideum, indicating that the protein family may modulate intracellular growth in a complex fashion. VipD is mildly toxic when overproduced in eukaryotic cells, and the toxicity is partially dependent on the putative phospholipase active site. VipD and its paralogs therefore define a family of translocated proteins that may assist in the establishment of a vacuole suitable for bacterial replication through functioning as a phospholipase.

Amino Acid Sequence↗

PubMed1992

Interaction of ethanol with signal transduction mechanisms mediating growth hormone release by rat pituitary cells in vitro.

The effects of ethanol on signal transduction mechanisms of rat GH (rGH) release were investigated in primary culture of rat anterior pituitary cells. Ethanol (30, 100, and 300 mM) had no significant effect on basal rGH release or cell content after a 4-h incubation or on intracellular cAMP levels at 30 min. Ethanol did not alter rGRH (10(-11) M)-stimulated rGH release, but at concentrations of 100 and 300 mM it inhibited rGRH (10(-9) M)-stimulated rGH release by 12% (P less than 0.05) and 54% (P less than 0.01). In contrast, a dose-dependent stimulatory effect was observed on rGRH-induced cAMP accumulation. Ethanol enhanced the inhibitory effect of SRIH (10(-11) and 10(-9) M) on rGH release by up to 24% (P less than 0.01). Stimulation of rGH release by cAMP derivatives and forskolin was partially inhibited by ethanol, as was cAMP accumulation after forskolin treatment. Cholera toxin-stimulated rGH release was also inhibited by ethanol, whereas cAMP accumulation was increased. At the higher concentrations, ethanol enhanced rGH release after protein kinase-C activation by phorbol ester and after stimulation of calcium influx with Ca ionophore. No significant ethanol effect was noted on prostaglandin E2-stimulated rGH release, and ethanol did not alter rGH mRNA levels or proliferation of a pituitary somatomammotroph cell line. The results indicate that ethanol exerts multiple effects on systems mediating GH release from the pituitary in vitro. However, the inhibitory influence of ethanol on GH secretion is related primarily to the adenylate cyclase-cAMP pathway, which represents the major signal transducing system in the somatotroph.

Animals↗

PubMed1982

Characterization of alpha-latrotoxin interaction with rat brain synaptosomes and PC12 cells.

alpha-latrotoxin, a polypeptide neurotoxin purified from the venom of the spider Latrodectus mactans tredecimguttatus, induces a massive release of a variety of neurotransmitters from rat brain synaptosomes and a clonal pheochromocytoma cell line (PC12 cells). In both systems secretion of catecholamines is dose- and calcium-dependent. Efflux of catecholamines is coupled with a substantial release of intracellular ATP. Independent of alpha-latrotoxin with PC12 cells is followed by a rapid influx of calcium and sodium ions, the rate being dependent on toxin and calcium concentrations. By reductive methylation it is possible to radioactively label alpha-latrotoxin without appreciable loss of neurotoxicity. A sensitive binding assay in vitro allows the identification of a limited number of specific binding sites in central nervous system synaptic membranes and PC12 cells, for which tritiated alpha-latrotoxin displays nanomolar affinity.

Adrenal Gland Neoplasms↗

PubMed2000

Identification of sat, an autotransporter toxin produced by uropathogenic Escherichia coli.

Urinary tract infection (UTI) is a very common extraintestinal infection, and Escherichia coli is by far the most common causative organism. Uropathogenic E. coli possess traits that distinguish them from commensal strains of E. coli, such as secretion systems that allow virulence factors to be targeted to extracytoplasmic compartments. One of at least five characterized secretion mechanisms is the autotransporter system, which involves translocation of a protein across the inner membrane, presumably via the sec system, and across the outer membrane through a beta-barrel porin structure formed by the carboxy-terminus autotransporter domain. We identified a 107 kDa protein that was expressed significantly more often by E. coli strains associated with the clinical syndrome of acute pyelonephritis than by faecal strains (P = 0.029). We isolated the protein from E. coli CFT073, a strain cultured from the blood and urine of a patient with acute pyelonephritis. The N-terminal amino acid sequence showed highest similarity to two known SPATE (serine protease autotransporters of Enterobacteriaceae) proteins, Pet and EspC. Using a 509 bp probe from the 5' region of pet, 10 cosmid clones of an E. coli CFT073 gene library were positive for hybridization. From one cosmid clone, a 7.5 kb EcoRI restriction fragment, which reacted strongly with the probe, was shown to include the entire 3885 bp gene. The predicted 142 kDa protein product possesses the three domains that are typical of SPATE autotransporters: an unusually long signal sequence of 49 amino acids; a 107 kDa passenger domain containing a consensus serine protease active site (GDSGSG); and a C-terminal autotransporter domain of 30 kDa. The protein exhibited serine protease activity and displayed cytopathic activity on VERO primary kidney, HK-2 bladder and HEp-2 cell lines; the name Sat (secreted autotransporter toxin) was derived from these properties. In addition, Sat antibodies were present in the serum of mice infected with E. coli CFT073. Based upon its association with pathogenic isolates, its cytopathic phenotype and its ability to elicit a strong antibody response after infection, we postulate that Sat represents a novel virulence determinant of uropathogenic E. coli.

Amino Acid Sequence↗

PubMed1998

An experimental prime-boost regimen leading to HIV type 1-specific mucosal and systemic immunity in BALB/c mice.

Induction of mucosal as well as systemic immunity to HIV-1 is considered to have high priority in current concepts of future AIDS vaccines. Here we show that the desired immune responses can be elicited by an experimental prime-boost regimen consisting of mucosal (intragastric) application of a recombinant vaccinia virus carrying the HIV-1 env gene (vSC25), followed by parenteral (intradermal) immunization with the recombinant HIV-1 glycoprotein 160 (rgp160). Following intragastric immunization of mice with vSC25 in combination with the mucosal adjuvant cholera toxin (CT), HIV-1 env-specific IgA was secreted by B cells of Peyer's patches and the lamina propria. Moreover, mucosal (intragastric and intranasal) application of vSC25 (both in presence or absence of CT) induced a long-lasting, HIV-1 env-specific systemic cytotoxic T cell response. Subsequent intradermal boosters with rgp160 led to HIV-1-specific T cell memory and serum antibodies.

AIDS Vaccines↗

PubMed1995

A new class of inhibitors of cAMP-mediated Cl- secretion in rabbit colon, acting by the reduction of cAMP-activated K+ conductance.

Previously we have shown that arylaminobenzoates like 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), which are very potent inhibitors of NaCl absorption in the thick ascending limb of the loop of Henle, are only poor inhibitors of the cAMP-mediated secretion of NaCl in rat colon. This has prompted our search for more potent inhibitors of NaCl secretion in the latter system. The chromanole compound 293 B inhibited the equivalent short-circuit current (Isc) induced by prostaglandin E2 (n = 7), vasoactive intestinal polypeptide (VIP, n = 5), adenosine (n = 3), cholera toxin (n = 4) and cAMP (n = 6), but not by ionomycin (n = 5) in distal rabbit colon half maximally (IC50) at 2 mumol/l from the mucosal and at 0.7 mumol/l from the serosal side. The inhibition was reversible and paralleled by a significant increase in transepithelial membrane resistance [e.g. in the VIP series from 116 +/- 16 omega.cm2 to 136 +/- 21 omega.cm2 (n = 5)]. A total of 25 derivatives of 293 B were examined and structure activity relations were obtained. It was shown that the racemate 293 B was the most potent compound within this group and that its effect was due to the enantiomer 434 B which acted half maximally at 0.25 mumol/l. Further studies in isolated in vitro perfused colonic crypts revealed that 10 mumol/l 293 B had no effect on the membrane voltage across the basolateral membrane (Vbl) in non-stimulated crypt cells: -69 +/- 3 mV versus -67 +/- 3 mV (n = 10), whilst in the same cells 1 mmol/l Ba2+ depolarised Vbl significantly. However, 293 B depolarised Vbl significantly in the presence of 1 mumol/l forskolin: -45 +/- 4 mV versus -39 +/- 5 mV (n = 7). Similar results were obtained with 0.1 mmol/l adenosine. 293 B depolarised Vbl from -40 +/- 5 mV to -30 +/- 4 mV (n = 19). This was paralleled by an increase in the fractional resistance of the basolateral membrane. VIP had a comparable effect. The hyperpolarisation induced by 0.1 mmol ATP was not influenced by 10 mumol/l 293 B: -75 +/- 6 mV versus -75 +/- 6 mV (n = 6). Also 293 B had no effect on basal K+ conductance (n = 4). Hence, we conclude that 293 B inhibits the K+ conductance induced by cAMP. This conductance is apparently relevant for Cl- secretion and the basal K+ conductance is insufficient to support secretion.

Amiloride↗

PubMed2004

Mucosally delivered Salmonella live vector vaccines elicit potent immune responses against a foreign antigen in neonatal mice born to naive and immune mothers.

The development of effective vaccines for neonates and very young infants has been impaired by their weak, short-lived, and Th-2 biased responses and by maternal antibodies that interfere with vaccine take. We investigated the ability of Salmonella enterica serovars Typhi and Typhimurium to mucosally deliver tetanus toxin fragment C (Frag C) as a model antigen in neonatal mice. We hypothesize that Salmonella, by stimulating innate immunity (contributing to adjuvant effects) and inducing Th-1 cytokines, can enhance neonatal dendritic cell maturation and T-cell activation and thereby prime humoral and cell-mediated immunity. We demonstrate for the first time that intranasal immunization of newborn mice with 10(9) CFU of S. enterica serovar Typhi CVD 908-htrA and S. enterica serovar Typhimurium SL3261 carrying plasmid pTETlpp on days 7 and 22 after birth elicits high titers of Frag C antibodies, previously found to protect against tetanus toxin challenge and similar to those observed in adult mice. Salmonella live vectors colonized and persisted primarily in nasal tissue. Mice vaccinated as neonates induced Frag C-specific mucosal and systemic immunoglobulin A (IgA)- and IgG-secreting cells, T-cell proliferative responses, and gamma interferon secretion. A mixed Th1- and Th2-type response to Frag C was established 1 week after the boost and was maintained thereafter. S. enterica serovar Typhi carrying pTETlpp induced Frag C-specific antibodies and cell-mediated immunity in the presence of high levels of maternal antibodies. This is the first report that demonstrates the effectiveness of Salmonella live vector vaccines in early life.

Administration, Intranasal↗

PubMed2005

Suppression of Drosophila cellular immunity by directed expression of the ExoS toxin GAP domain of Pseudomonas aeruginosa.

We show here that transgenic Drosophila can be used to decipher the effect of a bacterial toxin on innate immunity and demonstrate the contribution of blood cells in fly resistance to bacterial infection. ExoS is a Pseudomonas aeruginosa exotoxin directly translocated into the host cell cytoplasm through the type III secretion system found in many Gram-negative bacteria. It contains a N-terminal GTPase activating (GAP) domain that prevents cytoskeleton reorganization by Rho family of GTPases in cell culture. Directed expression of the ExoS GAP domain (ExoSGAP) during fly eye morphogenesis inhibited Rac1-, Cdc42- and Rho-dependent signalling, demonstrating for the first time its activity on RhoGTPases in a whole organism. We further showed that fly resistance to P. aeruginosa infections was altered when ExoSGAP was expressed either ubiquitously or in haemocytes, but not when expressed into the fat body, the major source of NF-(kappa)B-dependent anti-microbial peptide synthesis. Fly sensitivity to infection was also observed with Gram-positive Staphylococcus aureus strain and was associated to a reduced phagocytosis capacity of ExoSGAP-expressing haemocytes. Our results highlight the major contribution of cellular immunity during the first hours after Drosophila infection by P. aeruginosa, an opportunist pathogen affecting patients with pathologies associated to a reduced leukocyte number.

ADP Ribose Transferases↗

PubMed1985

Pertussis toxin potentiates anesthesia-induced renin secretion.

The plasma renin concentration was measured after anesthesia in control and in pertussis toxin-treated rats. The anesthetics increased renin secretion and this effect was markedly magnified in rats treated with pertussis toxin. Propranolol partially blocked the increase in plasma renin concentration produced by anesthetics. It is concluded that the adrenergic system is involved in this effect and that pertussis toxin magnifies it by potentiating the beta-adrenergic action.

Anesthesia↗

PubMed1982

Cytotonic enterotoxin from Aeromonas hydrophila.

Aeromonas hydrophila produces two hemolysins and an enterotoxin during growth. Enterotoxin, separated from the hemolysins, gave positive reactions in the rabbit intestinal loop test, the rabbit skin test and the adrenal Y1 cell test. Neutralization experiments in the rabbit loop, rabbit skin and Y1 cell tests failed to demonstrate any immunological relationship between Aeromonas enterotoxin and cholera toxin or Escherichia coli heat-labile enterotoxin. Prior incubation of Aeromonas enterotoxin with gangliosides did not inhibit the positive test results in these systems. A co-agglutination test with antiserum to purified cholera toxin was negative for Aeromonas enterotoxin, which therefore seems to be immunologically distinct from cholera toxin. The Aeromonas enterotoxin induced steroid secretion in adrenal Y1 cells and increased the intracellular cyclic adenosine monophosphate (cAMP) content of Y1 cells as well as of rabbit intestinal epithelial cells. It thus seems to act via the adenylate cyclase-cAMP pathway and should be classified as a cytotonic enterotoxin according to the classification of Keusch and Donta (1975).

Adenylyl Cyclases↗

PubMed1999

Type III machines of pathogenic yersiniae secrete virulence factors into the extracellular milieu.

Gram-negative bacteria use type III machines to inject toxic proteins into the cytosol of eukaryotic cells. Pathogenic Yersinia species export 14 Yop proteins by the type III pathway and some of these, named effector Yops, are targeted into macrophages, thereby preventing phagocytosis and allowing bacterial replication within lymphoid tissues. Hitherto, YopB/YopD were thought to insert into the plasma membrane of macrophages and to promote the import of effector Yops into the eukaryotic cytosol. We show here that the type III machines of yersiniae secrete three proteins into the extracellular milieu (YopB, YopD and YopR). Although intrabacterial YopD is required for the injection of toxins into eukaryotic cells, secreted YopB, YopD and YopR are dispensable for this process. Nevertheless, YopB, YopD and YopR are essential for the establishment of Yersinia infections in a mouse model system, suggesting that type III secretion machines function to deliver virulence factors into the extracellular milieu also.

Animals↗