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PubMedDate not supplied

Tumor immunogenicity--the prime determinant of the nutritional influence on the host-tumor relationship.

The influence which malnutrition plays on the host-tumor relationship is controversial because of the disparity of human and rodent tumors, a critical difference being the minimal immunogenicity of human tumors and the variable antigenicity of rodent tumors. The hypothesis we tested is that the influence of malnutrition on tumor growth is a result of the immunogenicity of the host's tumor. C-1300 neuroblastoma (NB) is an immunogenic tumor by in vivo and in vitro assessment while the histologically identical TBJ-NB clone is non-immunizing. Isogeneic A/J mice were malnourished with 2.5% protein chow and were inoculated with C-1300-NB or TBJ-NB; either serial tumor volumes were assessed by three-dimensional measurement or animals were serially killed and tumor weight/carcass weight ratios (TW/CW) were calculated. Non-immunogenic TBJ-NB grew more rapidly than C-1300-NB in both control and malnourished groups, but there was no difference in either tumor size or TW/CW ratios between the two TBJ-NB nutritional groups. Contrasting with these data were immunogenic C-1300-NB in that the tumor grew significantly better in malnourished mice (tumor volume p less than 0.05 day 12 and 14; TW/CW p less than 0.026 by day 21). Prior whole-body irradiation abrogated this difference. These data demonstrate that for tumors differing only in antigenicity the influence of malnutrition is on that tumor which induces an immunologic antitumor response.

Animals↗

PubMedDate not supplied

[Effect of Yersinia pseudotuberculosis pVM82 on the activity of components of complement and phagocytosis by human blood neutrophils].

Three isogenic Y. pseudotuberculosis strains were studied. One of them contained pVM82 plasmid which was found in foci of pseudotuberculosis outbreaks and increased Yersinia resistance to blood serum. Cells with pVM82 plasmid did not inhibit the activation of complement components C1, C2, C3, C4, and C5 in human serum and increased the consumption of these complement components in comparison with control strains. Y. pseudotuberculosis cells with pVM82 were better resistant to human neutrophil phagocytosis than bacterial cells without this plasmid. For the strain with pVM82 plasmid, a lower level of phagocytosis within the first 30 min of Y. pseudotuberculosis incubation with neutrophils and a reduced percentage of killed bacteria among all those phagocytosed over the entire period of incubation of bacteria with neutrophils were observed.

Complement System Proteins↗

PubMed2004

Identification of sarV (SA2062), a new transcriptional regulator, is repressed by SarA and MgrA (SA0641) and involved in the regulation of autolysis in Staphylococcus aureus.

The expression of genes involved in the pathogenesis of Staphylococcus aureus is known to be controlled by global regulatory loci, including agr, sarA, sae, arlRS, lytSR, and sarA-like genes. Here we described a novel transcriptional regulator called sarV of the SarA protein family. The transcription of sarV is low or undetectable under in vitro conditions but is significantly augmented in sarA and mgrA (norR or rat) (SA0641) mutants. The sarA and mgrA genes act as repressors of sarV expression, as confirmed by transcriptional fusion and Northern analysis data. Purified SarA and MgrA proteins bound specifically to separate regions of the sarV promoter as determined by gel shift and DNase I footprinting assays. The expression of 19 potential target genes involved in autolysis and virulence, phenotypes affected by sarA and mgrA, was evaluated in an isogenic sarV mutant pair. Our data indicated that the sarV gene product played a role regulating some virulence genes and more genes involved in autolysis. The sarV mutant was more resistant to Triton X-100 and penicillin-induced lysis compared to the wild type and the sarA mutant, whereas hyperexpression of sarV in the parental strain or the sarV mutant rendered the resultant strain highly susceptible to lysis. Zymographic analysis of murein hydrolase activity revealed that inactivation of the sarV gene results in decreased extracellular murein hydrolase activity compared to that of wild-type S. aureus. We propose that sarV may be part of the common pathway by which mgrA and sarA gene products control autolysis in S. aureus.

Animals↗

PubMed1989

Ducto-insular proliferation of beta-cells after syngeneic islet transplantation into the spleen of streptozotocin-diabetic Lewis rats.

Syngeneic transplantation of cultured and functionally characterized neonatal islets into the spleen of streptozotocin diabetic Lewis rats resulted in long time survival up to 200 d and in plasma glucose levels lower than 9 mmol/L. The daily plasma glucose profile of transplanted rats had shown significantly above that of nondiabetic control rats. Two-hundred d after transplantation, morphologically intact, insulin containing beta-cells were demonstrable in the spleen, thus demonstrating the long-term survival of functioning islet cells. Proliferation of beta-cells was shown in the transplanted islets. In addition, beta-cell clusters were found that derived from pancreatic ductules transplanted together with the isolated islets into the spleen. Mitoses were visible within ductular epithelial cells. The proliferative response of islets after intrasplenic transplantation is probably the result of a long-term stimulation by slightly enhanced plasma glucose values of the transplant acceptors compared to control animals.

Animals↗

PubMed1998

Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice.

Secreted forms of the beta-amyloid precursor protein (beta-APP) have neuroprotective properties in vitro and may be involved in the containment of neuronal excitation. To test whether loss of secreted forms of beta-APP (sAPPs) may enhance excitotoxic responses, we injected mice homozygous for a targeted mutation of the beta-APP gene (beta-APPDelta/Delta) intraperitoneally with kainic acid. We found that in these mice, kainic acid induced seizures initiated earlier, and acute mortality was enhanced compared to isogenic wild-type mice independently from the callosal agenesis phenotype observed to occur at increased frequency in APP mutant mice. Expression of c-fos in cortex and cingulate gyrus was enhanced in beta-APPDelta/Delta mice, although the amount of structural damage and apoptosis in the hippocampal pyramidal cell layer and cortex was similar to that of controls. When cerebellar granule cell cultures and cortical neuronal cultures were challenged with glutamate receptor agonists, the rates of cell death and apoptosis of beta-APPDelta/Delta mice were indistinguishable from those of controls. Therefore, deficiency of sAPPs causes facilitation of seizure activity in the absence of enhanced cell death. Since enhanced seizures were observed also in mice homozygous for a deletion of the entire beta-APP gene, this phenotype results from a loss of APP rather than from a dominant effect of APPDelta.

Amyloid beta-Protein Precursor↗

PubMed2003

Quorum-sensing control of biofilm factors in Staphylococcus epidermidis.

Staphylococcus epidermidis is the most frequent cause of nosocomial sepsis and catheter-related infections, in which biofilm formation is considered to be the main virulence mechanism. Quorum-sensing systems have been recognized as important regulators of virulence and biofilm formation in many bacteria. There is a single quorum-sensing system in S. epidermidis encoded by the agr operon. To investigate quorum-sensing control of biofilm formation, we constructed an agr deletion mutant, assayed for the different stages of biofilm formation, and determined agr-dependent regulation of biofilm factors. The agr mutant showed increased biofilm formation, primary attachment, and expression of the autolysin AtlE, but lacked delta-toxin production. However, the level of polysaccharide intercellular adhesin expression was equivalent to the isogenic wild-type strain. In contrast to AtlE, which is known to influence primary attachment, delta-toxin appeared to exert its effect on attachment to polystyrene during later stages of biofilm formation. Importantly, addition of cross-inhibiting pheromones mimicked an agr mutation and significantly enhanced biofilm formation, which suggests that care should be used when treating S. epidermidis infections with cross-inhibiting peptides. Our data demonstrate the importance of quorum sensing in the establishment of a biofilm in this critical human pathogen.

Bacterial Adhesion↗

PubMed1983

In vivo and in vitro binding of iodinated monoclonal antibody A2B5 to RIN insulinoma cells.

Monoclonal antibody A2B5 reacts with the cell surface of a series of amine precursor uptake decarboxylation (APUD) cells and their tumors in many vertebrate species including chicken, rat, mouse, and man. We have studied the in vivo and in vitro binding of iodinated monoclonal antibody A2B5 to rat insulinoma cells. In vitro, radiolabeled A2B5 binds specifically to RINm5F insulinoma cells and the binding of 125I-A2B5 is inhibited by unlabeled A2B5 or a ganglioside extract of RINm5F cells. In vivo, scintigrams taken Day 0 to Day 5 after injection of 131I-labeled A2B5 showed a striking localization of 131I-A2B5 in transplanted RIN tumors grown in syngeneic rats. Other control radiolabeled monoclonal antibodies did not concentrate in the tumors. 131I-labeled A2B5 did not concentrate in other transplantable tumors (colon adenocarcinoma, osteosarcoma, renal cell carcinoma, and bladder transitional cell carcinoma) grown in nude mice. The tumor/blood ratio detected 5 days after antibody injection, was approximately two to 12 times higher in the insulinoma compared to other organs and only in the insulinoma did 131I-A2B5 show a higher concentration than control antibody 125I-P3X63.

Adenoma, Islet Cell↗

PubMed2001

The role of p21(CIP1/WAF1) in growth of epithelial cells exposed to hyperoxia.

Previous studies have shown that hyperoxia inhibits proliferation and increases the expression of the tumor suppressor p53 and its downstream target, the cyclin-dependent kinase inhibitor p21(CIP1/WAF1), which inhibits proliferation in the G1 phase of the cell cycle. To determine whether growth arrest was mediated through activation of the p21-dependent G1 checkpoint, the kinetics of cell cycle movement during exposure to 95% O2 were assessed in the Mv1Lu and A549 pulmonary adenocarcinoma cell lines. Cell counts, 5-bromo-2'-deoxyuridine incorporation, and cell cycle analyses revealed that growth arrest of both cell lines occurred in S phase, with A549 cells also showing evidence of a G1 arrest. Hyperoxia increased p21 in A549 but not in Mv1Lu cells, consistent with the activation of the p21-dependent G1 checkpoint. The ability of p21 to exert the G1 arrest was confirmed by showing that hyperoxia inhibited proliferation of HCT 116 colon carcinoma cells predominantly in G1, whereas an isogenic line lacking p21 arrested in S phase. The cell cycle arrest in S phase appears to be a p21-independent process caused by a gradual reduction in the rate of DNA strand elongation. Our data reveal that hyperoxia inhibits proliferation in G1 and S phase and demonstrate that p53 and p21 retain their ability to affect G1 checkpoint control during exposure to elevated O2 levels.

Adenosine Triphosphate↗

PubMed2002

[Identification of quantitative trait loci controlling F2 sterility and heading date in rice].

Ninety-six F2 lines derived from a cross between a japonica cultivar Taichung 65 and an indica cultivar Bhadua were developed. At the first step, an RFLP linkage map based on the F2 lines was constructed. The RFLP map contained 94 RFLP makers. F2 sterility and heading date are important agronomic traits of rice; meanwhile heading date is related to many characters of agronomic importance including sterility. Quantitative trait locus (QTL) analysis was carried out to identify genes controlling F2 sterility and heading date. Both single factor analysis and interval analysis were applied for QTL analysis. Two QTLs for F2 spikelet sterility were newly detected on Chromosome 1 and 8. Five QTLs for heading date were detected on Chromosome 1, 4, 6, 8 and 10. Two of them on chromosome 1 and 10 were newly detected. Near-isogenic lines are now under construction for further QTL analysis and gene mapping of these QTLs newly identified in this paper.

Chromosome Mapping↗

PubMed1990

[Proliferation of beta cells after syngeneic transplantation of isolated Langerhans cells into the spleens of diabetic rats].

Syngeneic transplantation of cultured and functionally characterized neonatal islet into the spleen of streptozotocin diabetic Lewis rats resulted in long time survival up to 200 days and in plasma glucose levels lower than 9 mmol/l. The daily plasma glucose profile of transplanted rats had shown significantly above that of non diabetic control rats. 200 days after transplantation morphologically intact, insulin containing beta-cells were demonstrable in the spleen, thus demonstrating the long-term survival of functioning islet cells. Proliferation of beta-cells was shown in the transplanted islets. In addition, beta-cell clusters were found which derived from pancreatic ductules transplanted together with the isolated islets into the spleen. Mitose were visible within ductular epithelial cells. The proliferative response of islets after intrasplenic transplantation is probably the result of a long-term stimulation by slightly enhanced plasma glucose values of the transplanted acceptors compared to control animals.

Animals↗

PubMed1987

In vivo studies on allotolerance perimetamorphically induced in control and thymectomized Xenopus.

Implantation of either major histocompatibility complex (MHC)-disparate thymus to 7-day thymectomized (Tx) Xenopus in late larval life, or allogeneic skin to perimetamorphic controls, routinely induces tolerance towards implant-strain skin grafts applied in adult life. To characterize this allotolerance further, additional in vivo approaches were attempted. Injection of gamma-irradiated (5000 rads) implant-strain splenocytes into frogs bearing tolerant skin grafts revealed (within 3 days) significantly elevated tritiated thymidine uptake by host spleen cells, compared to siblings injected with isogeneic cells. Although this in vivo 'mixed leucocyte reaction' proved to be thymus dependent, the identity of the cells involved awaits clarification. When non-restored Tx Xenopus are injected with live MHC-disparate splenocytes, graft-versus-host (GVH)-induced mortality ensued within 2 weeks. Such GVH disease also occurred (albeit more chronically) when Tx allothymus-implanted animals were given MHC-incompatible splenocytes, but only when these came from the thymus donor strain. Splenocytes from thymus-implanted animals failed to achieve GVH-induced splenomegaly when transferred to appropriate hosts (bearing MHC antigens of the thymus donor strain). Overall, the experiments indicate that alloreactivity against donor cells is impaired but not completely inhibited in Xenopus following perimetamorphic implantation.

Animals↗

PubMed1987

Responses of serum from breast cancer patients to murine mammary tumor virus: fact or artifact?

For determination of whether breast cancer patients possessed specific serological responses to murine mammary tumor virus (MuMTV), IgG-binding levels were monitored by antibody binding to electrophoretically separated viral proteins (Western blotting and immunodetection) and by the enzyme-linked immunosorbent assay (ELISA) against a panel of five structural proteins (gp55, gp34, p28, p18, and p12) purified from milk-borne MuMTV of the RIII isogeneic mouse strain. No significant antibody reactions were found for sera from 30 cancer patients by the immunoblotting assay, and comparative ELISA studies of 111 patients with malignant mastopathies and 122 healthy, age-matched women revealed no significantly increased mean antibody responses against gp55, gp34, p28, or p12 in breast cancer patients as compared to the responses in the control group. Only for p18 was there a significant increase in mean IgG-binding levels in cancer patients. Additional assays of antibody binding to viral antigens were performed by the cellular immunofluorescence test on MuMTV-expressing cells. These studies also failed to demonstrate greater immunoreactivity of sera from patients as opposed to the immunoreactivity of sera from healthy controls.

Adolescent↗

PubMed1988

Quantitative transplantation assays of spontaneous tumors of the C3H mouse as allografts in athymic NCr/Sed-nu/nu nude mice and isografts in C3Hf/Sed mice.

Three spontaneous tumors of the C3H mouse have been used in a comparison of their transplantability and radiation response (local control) in syngeneic C3Hf/Sed mice and in allogeneic athymic NCr/Sed-nu/nu nu nude mice. The tumors were: MCaIV, a moderately well-differentiated mammary carcinoma; FSaII, a poorly differentiated fibrosarcoma; and SCCVII, a moderately well differentiated squamous cell carcinoma. The tumors were studied as fourth to seventh generation transplants. Assays to determine the number of tumor cells that, on the average, transplant the tumor to half of the recipients or transplant sites (TD50) demonstrated that these 3 tumors transplanted into the s.c. tissue of the NCr/Sed-nu/nu as readily as of C3Hf/Sed mice. The TD50 for MCaIV was slightly but significantly lower in 4-week-old NCr/Sed-nu/nu mice which had received 6 Gy whole body irradiation (WBI) 24 h before transplantation, namely, 5.8 x 10(4) (95% confidence limits, 4.5-7.6) versus 7.8 x 10(4) (6.0-10.0). The 6-Gy WBI did not affect the TD50 for 8- to 10-week-old mice. Similarly, the TD50 for SCCVII was lower in 6-Gy WBI NCr/Sed-nu/nu recipients (1.5 x 10(4) versus 3.9 x 10(4)). The TD50 for FSaII was not affected by 6-Gy WBI. Further, the TD50 for FSaII following i.v. injection of tumor cells (transplant to lung) was the same for C3Hf/Sed and NCr/Sed-nu/nu mice (this obtained for normal or 6-Gy WBI-treated subjects). The radiation doses which on the average achieve control of half of the MCaIV, FSaII, and SCCVII tumors were lower, higher, and the same in NCr/Sed-nu/nu than in C3Hf/Sed mice, respectively. The radiation doses which achieve control of half of the MCaIV and SCCVII tumors were not affected by 6-Gy WBI before transplantation.

Animals↗

PubMed1996

The S. cerevisiae nitrogen starvation-induced Yvh1p and Ptp2p phosphatases play a role in control of sporulation.

Starvation for nitrogen in the absence of a fermentable carbon source causes diploid Saccharomyces cerevisiae cells to leave vegetative growth, enter meiosis, and sporulare; the former nutritional condition also induces expression of the YVH1 gene that encodes a protein phosphatase. This correlation prompted us to determine whether the Yvh1p phosphatase was a participant in the network that controls the onset of meiosis and sporulation. We found that expression of the IME2 gene, encoding a protein kinase homologue required for meiosis- and sporulation-specific gene expression, is decreased in a yvh1 disrupted strain. We also observed a decrease, albeit a smaller one, in the expression of IME1 which encodes an activator protein required for IME2 expression. Under identical experimental conditions, expression of the MCKI and IME4 genes (which promote sporulation but do not require Ime1p for expression) was not affected. These results demonstrate the specificity of the yvh1 disruption phenotype. They suggest that decreased steady-state levels of IME1 and IME2 mRNA were not merely the result of non-specific adverse affects on nucleic acid metabolism caused by the yvh1 disruption. Sporulation of a homozygous yvh1 disruption mutant was delayed and less efficient overall compared to an isogenic wild-type strain, a result which correlates with decreased IME1 and IME2 gene expression. We also observed that expression of the PTP2 tyrosine phosphatase gene (a negative regulator of the osmosensing MAP kinase cascade), but not the PTP1 gene (also encoding a tyrosine phosphatase) was induced by nitrogen-starvation. Although disruption of PTP2 alone did not demonstrably affect sporulation or IME2 gene expression, sporulation was decreased more in a yvh1, ptp2 double mutant than in a yvh1 single mutant; it was nearly abolished in the double mutant. These data suggest that the YVH1 and PTP2 encoded phosphatases likely participate in the control network regulating meiosis and sporulation. Expression of YVH1 and PTP2 was not affected by nitrogen source quality (asparagine compared to proline) suggesting that nitrogen starvation-induced YVH1 and PTP2 expression and sensitivity to nitrogen catabolite repression are on two different branches of the nitrogen regulatory network.

Cell Cycle Proteins↗

PubMed1998

Differential temperature modulation by H-NS of the fimB and fimE recombinase genes which control the orientation of the type 1 fimbrial phase switch.

Phase variation of type 1 fimbriation in Escherichia coli is associated with the inversion of a 314-bp DNA element. This DNA switch directs transcription of fimA, encoding the major type 1 fimbrial subunit, in the on orientation but not in the off orientation. Inversion of the DNA element requires either FimB (confers both on and off orientations) or FimE (confers off orientation). Here we show, by chromosomally located fimB- and fimE-lacZ cassettes in isogenic strain sets differing only in the hns locus, how the global regulator H-NS affects the expression of type 1 fimbriae. H-NS was found to downregulate fimB and fimE in a temperature-dependent manner which affected the genes inversely at 30 degrees C and 37 degrees C. By gel-retardation assays H-NS binding was demonstrated to the regions containing the fimB promoter and the fimE promoter, respectively. In vitro recombination analysis suggested no direct involvement of H-NS in the inversion of the phase switch. Rather than directly affecting the switching process per se, it appeared that the orientation of this element was affected by the differential temperature modulation of H-NS of the fimB and fimE genes. Taken together the results suggest that H-NS modulates expression of type 1 fimbriae in a way which seems to favor a fimbriate state at the mammalian body temperature.

Bacterial Proteins↗

PubMed2001

Iron-dependent transcription of the frpB gene of Helicobacter pylori is controlled by the Fur repressor protein.

We have overexpressed and purified the Helicobacter pylori Fur protein and analyzed its interaction with the intergenic regions of divergent genes involved in iron uptake (frpB and ceuE) and oxygen radical detoxification (katA and tsaA). DNase I footprint analysis showed that Fur binds specifically to a high-affinity site overlapping the P(frpB) promoter and to low-affinity sites located upstream from promoters within both the frpB-katA and ceuE-tsaA intergenic regions. Construction of an isogenic fur mutant indicated that Fur regulates transcription from the P(frpB) promoter in response to iron. In contrast, no effect by either Fur or iron was observed for the other promoters.

Bacterial Outer Membrane Proteins↗

PubMed2002

Mapping QTLs regulating morpho-physiological traits and yield: case studies, shortcomings and perspectives in drought-stressed maize.

Comparative analysis of a number of studies in drought-stressed maize (Zea mays L.) reporting quantitative trait loci (QTLs) for abscisic acid concentration, root characteristics, other morpho-physiological traits (MPTs) and grain yield (GY) reveals their complex genetic basis and the influence of the genetic background and the environment on QTL effects. Chromosome regions (e.g. near umc11 on chromosome 1 and near csu133 on chromosome 2) with QTLs controlling a number of MPTs and GY across populations and conditions of different water supply have been identified. Examples are presented on the use of QTL information to elucidate the genetic and physiological bases of the association among MPTs and GY. The QTL approach allows us to develop hypotheses accounting for these associations which can be further tested by developing near isogenic lines (NILs) differing for the QTL alleles. NILs also allow for a more accurate assessment of the breeding value of MPTs and, in some cases, may allow for the map-based cloning of the gene(s) underlying the QTL. Although QTL analysis is still time-consuming and resource-demanding, its integration with genomics and post-genomics approaches (e.g. transcriptome, proteome and metabolome analyses) will play an increasingly important role for the identification and validation of candidate genes affecting MPTs and GY.

Abscisic Acid↗

PubMed1988

marA locus causes decreased expression of OmpF porin in multiple-antibiotic-resistant (Mar) mutants of Escherichia coli.

Mar (multiple antibiotic resistant) mutants of Escherichia coli express chromosomally mediated resistance to a variety of structurally unrelated hydrophilic and hydrophobic antibiotics. Insertion of transposon Tn5 into the marA locus at min 34.05 on the chromosome completely reverses the Mar phenotype (A. M. George and S. B. Levy, J. Bacteriol. 155:531-540, 1983). We found that among changes in the outer membrane of Mar mutants, porin OmpF was greatly reduced, although Mar mutants were more resistant than cells lacking only OmpF. Transduction of the marA region from a Mar strain, but not a wild-type strain, led to loss of OmpF. P1 transduction of marA::Tn5 into a Mar mutant partially restored OmpF levels. Therefore, OmpF reduction required a mutation in the marA region. Mar mutants of an ompF-lacZ operon fusion strain expressed 50 to 75% of the beta-galactosidase activity of the isogenic non-Mar parental strain, while Mar mutants of a protein fusion strain expressed less than 10% of the enzyme activity in the non-Mar strain. These changes were completely reversed by insertion of marA::Tn5. The responsiveness of OmpF-LacZ to osmolarity and temperature changes was similar in Mar and wild-type strains. Although some transcriptional control may have been present, OmpF reduction appeared to occur primarily by a posttranscriptional mechanism. The steady-state levels of ompF mRNA were twofold lower and the mRNA was five times less stable in the Mar mutant than in the wild-type strain. Expression of micF, which lowers ompF mRNA levels, was elevated in Mar strains, as revealed by a micF-lacZ fusion. Studies with strains deleted for the micF locus showed that the marA-dependent reduction of OmpF required an intact micF locus. Our findings suggest that the marA locus directly or indirectly increases micF expression, causing a posttranscriptional decrease in ompF mRNA and reduced amounts of OmpF.

Bacterial Outer Membrane Proteins↗