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Query: UNIPROT:P06889 (Mol)
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In the studies of experimental salmonellosis, immunization of mice with a live vaccine SER of S. enteritidis was found to be effective against further infection with virulent S. enteritidis 116--54. Macrophages obtained from the peritoneal cavity, subcutaneous tissue or liver of immunized mice inhibited intracellular growth of bacteria and resisted cell degeneration caused by engulfment of virulent 116--54 bacteria. This immunity was called cellular immunity. We discovered by chance in 1961 a transfer agent of immunity (TA) from the culture fluid of immunized macrophages. This agent is RNA in nature and can be extracted from the spleen, peritoneal exudate cells or the lymph node of immunized animals and is called immune (i) RNA. We could demonstrate antibody activity in macrophages treated in vitro or in vivo with iRNA by the immune adherence hemagglutination technique. Cellulr immunity against tumor cells could be transferred in vitro or in vivo to lymphocytes through iRNA prepared from the spleen cells of syngeneic, allogeneic and xenogeneic animals immunized with the tumor cells. We prepared iRNA against antigens capable of inducing humoral antibody production in animals, i.e., RBCs, bacterial toxin, bacterial flagella and hapten-protein conjugates. Serum antibody was not demonstrated in recipient animals of iRNA's by single or repeated injections of these agents. However, in these animals an increase in the number of specific antibody-carrying cells was found as rosette-formers. It was found further that prior injection of iRNA could induce immunologic memory and produced a high titer of humoral antibody after a boosting stimulation with a small dose of the corresponding antigen. The required interval between the first iRNA and the second antigenic stimulation, and the minimal effective doses of iRNA and antigen are described. We studied the interaction of iRNA with either T- or B-cells and with both cells using adoptive transfer system, athymic nude mice and neonatally thymectomized (NT) mice. Immune rna's against T-dependent and T-independent antigens could not induce the proliferation of antibody-carrying cells in cyclophosphamide-treated (B-cell depleted) mice. But these agents could induce the proliferation of rosette-formers, implying that iRNA's can replace some role of T-cells even against T dependent antigens. B-cells can be directly activated by treatment with iRNA against both T-dependent and T-independnet antigens, and they differentiated into rosette-formers. Passive transfers of iRNA were successful in establishing immunity against infection with S. enteritidis, or immunity to Salmonella flagella, RBCs and hapten-protein conjugates. The ability of iRNA to confer a secondary response of antibody formation is serially and passively transmissible in recipient animals. These facts suggest the presence of some mechanism that is responsible for the amplification of antigenic stimulation in the immune response...
Mol Cell Biochem 1978 Aug 16
PMID:Ribonucleic acid in the immune response. 8 65

Salmonellosis is the most frequently reported foodborne illness in the United States, with Salmonella enteritidis being the leading cause of these outbreaks. Nucleotide sequence comparisons of the Salmonella plasmid virulence (spv) genes of S. enteritidis with those of S. typhimurium and S. dublin have revealed that a single base-pair change unique to S. enteritidis is present in the spvA gene. An 18-base synthetic oligonucleotide probe (SE-probe) that is completely homologous to the spvA gene of S. enteritidis but which has one base pair mismatch with other salmonellae was shown to be specific for S. enteritidis. In colony hybridization blots, 129 isolates of S. enteritidis, 29 other species of Salmonella, and 17 non-Salmonella spp. were tested with the SE-probe. The SE-probe hybridized with 96% of the S. enteritidis strains tested but did not react with the other Salmonella or non-Salmonella strains. These data suggest that the SE-probe can be used in a specific and rapid detection assay for S. enteritidis.
Mol Cell Probes 1995 Feb
PMID:DNA probe for detecting Salmonella enteritidis in food. 776 Aug 65

Genotypes were analysed within 30 isolates of Salmonella bovismorbificans from human or bovine salmonellosis and from environmental or food sources. Three clonal evolutionary lines (chromosomal genotypes) were identified on the basis of restriction fragment length polymorphism at the 16S rRNA genes, total protein profiles, and the location and copy number of a Salmonella-specific DNA insertion sequence, IS200. The predominant type was found with and without a 90 kbp plasmid homologous to the spv BC genes of S. typhimurium, and seven plasmid profiles were observed in this chromosomal genotype. This is the first such virulence plasmid to be reported in S. bovismorbificans. One example was found of two other clones which differed substantially from the predominant clone and from each other in chromosomal genotype. These results show that three clonal lines share the antigen profile of S. bovismorbificans, and provide a subtyping scheme for this serovar.
Mol Cell Probes 1993 Feb
PMID:Molecular genotype analysis of Salmonella bovismorbificans. 809 64

Multiple tandem copies of an immunogenic epitope comprising amino acids 8-23 of glycoprotein D of herpes simplex virus (HSV) were expressed as C-terminal fusions to tetanus toxin fragment C (TetC) in different Salmonella typhimurium live vaccine strains. Expression of the longer fusions was best in strains harbouring a lesion in htrA, a stress protein gene. SL3261, an aroA strain, did not effectively express the longer fusions. Mice immunised with an S. typhimurium C5 htrA mutant expressing fusions with two or four copies of the peptide made an antibody response to both the peptide and TetC, whereas constructs expressing one copy of the peptide only elicited antibody to TetC. A non-immunogenic octameric fusion underwent rearrangements in vivo resulting in a predominantly monomeric fusion. In contrast, the S. typhimurium SL3261 aroA vaccine expressing the TetC-tetrameric fusion did not elicit antibody to the peptide. Sera from mice immunised with a single dose of the dimer and tetramer fusions in the htrA strain neutralised HSV in vitro, and the mice were protected from HSV infection as measured by a reduction in virus load in the ear pinna. We have previously shown that mice vaccinated with salmonella expressing TetC are protected against tetanus toxin and virulent salmonella challenge. These results suggest that it may be possible to develop a multivalent vaccine against salmonellosis, tetanus and HSV.
Mol Microbiol 1996 Feb
PMID:A Salmonella typhimurium htrA live vaccine expressing multiple copies of a peptide comprising amino acids 8-23 of herpes simplex virus glycoprotein D as a genetic fusion to tetanus toxin fragment C protects mice from herpes simplex virus infection. 882 Jun 49

The alternative sigma factor RpoS (sigma S) is required for Salmonella virulence in mice. We report the immunizing capacity of Salmonella typhimurium rpoS and rpoS aroA mutants to protect susceptible BALB/c mice against subsequent oral challenge with virulent S. typhimurium. When administered orally or intraperitoneally, rpoS derivatives of the mouse-virulent S. typhimurium strains, C52 and SL1344, were highly attenuated and were efficient single-dose live vaccines. rpoS aroA mutants were more attenuated than corresponding single aroA or rpoS mutants, as assessed after oral or intraperitoneal administration, but retained significant ability to protect mice against salmonellosis. Salmonella rpoS and rpoS aroA mutants therefore deserve serious consideration for rational vaccine design. Consistent with this, Salmonella typhi Ty2, a 'wild-type' strain used widely for the development of human live-vaccine candidates against typhoid fever, was shown to be defective for rpoS. In addition, our results demonstrate that rpoS not only controls the growth and persistence of S. typhimurium in deep lymphoid organs, but also plays a role during the initial stages of oral infection.
Mol Microbiol 1996 Oct
PMID:Virulence and vaccine potential of Salmonella typhimurium mutants deficient in the expression of the RpoS (sigma S) regulon. 889 17

Salmonella infections in naturally susceptible mice grow rapidly, with death occurring only after bacterial numbers in vivo have reached a high threshold level, commonly called the lethal load. Despite much speculation, no direct evidence has been available to substantiate a role for any candidate bacterial components in causing death. One of the most likely candidates for the lethal toxin in salmonellosis is endotoxin, specifically the lipid A domain of the lipopolysaccharide (LPS) molecule. Consequently, we have constructed a Salmonella mutant with a deletion-insertion in its waaN gene, which encodes the enzyme that catalyses one of the two secondary acylation reactions that complete lipid A biosynthesis. The mutant biosynthesizes a lipid A molecule lacking a single fatty acyl chain and is consequently less able to induce cytokine and inducible nitric oxide synthase (iNOS) responses both in vivo and in vitro. The mutant bacteria appear healthy, are not sensitive to increased growth temperature and synthesize a full-length O-antigen-containing LPS molecule lacking only the expected secondary acyl chain. On intravenous inoculation into susceptible BALB/c mice, wild-type salmonellae grew at the expected rate of approximately 10-fold per day in livers and spleens and caused the death of the infected mice when lethal loads of approximately 10(8) were attained in these organs. Somewhat unexpectedly, waaN mutant bacteria grew at exactly the same rate as wild-type bacteria in BALB/c mice but, when counts reached 10(8) per organ, mice infected with mutant bacteria survived. Bacterial growth continued until unprecedentedly high counts of 10(9) per organ were attained, when approximately 10% of the mice died. Most of the animals carrying these high bacterial loads survived, and the bacteria were slowly cleared from the organs. These experiments provide the first direct evidence that death in a mouse typhoid infection is directly dependent on the toxicity of lipid A and suggest that this may be mediated via pro-inflammatory cytokine and/or iNOS responses.
Mol Microbiol 1998 Jul
PMID:A lethal role for lipid A in Salmonella infections. 972 Aug 73

Salmonella spp. interact with ileal mucosa and disrupt normal intestinal function, which results in an acute inflammatory cell influx, fluid secretion and enteritis. We have recently characterized SopB, a novel secreted effector protein of Salmonella dublin, and presented evidence that SopB is translocated into eukaryotic cells via a sip-dependent pathway to promote fluid secretion and inflammatory responses. Here, we show that sopB is located on a large DNA fragment unique to the Salmonella chromosome. This locus is conserved in Salmonella and maps at approximately 20 centisome of the S. typhimurium chromosome. Sequence analysis revealed that this Salmonella-specific DNA fragment is flanked by DNA sequences with significant sequence similarity to the Escherichia coli K-12 genes, tRNA1ser (serT) on one side and copS/copR on the other. Thus, this Salmonella-specific DNA fragment has features characteristic of 'pathogenicity islands' and, therefore, it was denoted SPI-5 (Salmonella pathogenicity island-5). SPI-5 was sequenced and was found to contain five novel genes, pipA, pipB, pipC, pipD (pathogenicity island-encoded proteins) and orf, in addition to sopB. The effect of mutations in pipA, pipB and pipD on the induction of fluid secretion and an acute inflammatory cell influx was assessed in bovine ligated ileal loops. The effect of mutations in SPI-5-encoded genes on systemic salmonellosis was assessed in mice. The results of these experiments suggest that SPI-5-encoded genes contribute to enteric but not to systemic salmonellosis.
Mol Microbiol 1998 Aug
PMID:Identification of a pathogenicity island required for Salmonella enteropathogenicity. 972 26

The Sudan plated lizard (Gerrhosaurus major), previously reported to be an afebrile species, was utilized in a series of experiments to test for various aspects of the acute phase response. Treatment of individuals with the antibiotic Baytril resulted in a slight (0.5 degree C) but significant reduction in mean selected body temperature (MSBT), while treatment with saline did not lower MSBT. Nonantibiotic treatment individuals had depressed plasma iron levels (86.6 +/- 22.4 micrograms Fe 100 ml-1 plasma) and treatment with Baytril produced a significant increase in plasma iron concentration (186.8 +/- 19.5 micrograms Fe 100 ml-1 plasma). Necropsy of randomly selected individuals indicated that animals obtained from the commercial supplier had Aeromonas, Arthrobacter, Pseudomonas and Salmonella infections and antibiotic treatment eliminated these infections. The growth rate of Aeromonas sobria is reduced when the bacteria are grown at 32 degrees C and reduced iron concentration compared to 34.5 degrees C and low iron concentration, which suggests that a fever response may not be beneficial in reducing bacterial growth. Saline injected, bacteria injected and antibiotic injected Gerrhosaurus major have high plasma zinc concentrations compared to the previously studied febrile species, Dipsosaurus dorsalis. This difference suggests that zinc concentrations in afebrile species deserve further study.
Comp Biochem Physiol A Mol Integr Physiol 1998 Jun
PMID:The acute phase response in the Sudan plated lizard, Gerrhosaurus major. 977 12

Two large virulence loci encoding type III secretion systems are present on the chromosome of Salmonella typhimurium. Salmonella pathogenicity island 2 (SPI2) is important for the survival of S. typhimurium in host organs and forms an insertion of about 40 kb at the tRNA(Val) gene. However, several indications suggested that SPI2 was not the result of a single event of horizontal gene transfer. We characterized the portion of SPI2 towards the 30 cs boundary and performed mutational analysis to investigate the contribution of this region to S. enterica virulence. This analysis indicates that SPI2 may be composed of at least two different genetic elements. About 15 kb of the 40 kb of SPI2 contain genes without a significant contribution to systemic infections in the model of murine salmonellosis. Our study allowed us to define genes in SPI2 important for virulence further and indicated that this locus has a complex mosaic structure.
Mol Microbiol 1999 Jan
PMID:Molecular and functional analysis indicates a mosaic structure of Salmonella pathogenicity island 2. 1002 66

During infection of its hosts, Salmonella enterica serovar Typhimurium (S. typhimurium) enters the epithelial cells of the small intestine. This process requires a number of invasion genes encoded on Salmonella pathogenicity island 1 (SPI1), a 40 kb stretch of DNA located near minute 63 of the S. typhimurium chromosome. Expression of S. typhimurium SPI1 invasion genes is activated by the transcription factor HilA. hilA is tightly regulated in response to many environmental conditions, including oxygen, osmolarity and pH. Regulation of hilA expression may serve to limit invasion gene expression to the appropriate times during Salmonella infection. We have mapped the transcription start site of hilA and identified regions of the promoter that are required for the repression of hilA expression by conditions unfavourable for Salmonella invasion. We have also identified two SPI1-encoded genes, hilC and hilD, that can independently derepress hilA expression. HilC and HilD are both members of the AraC/XylS family of transcriptional regulators. A mutation in hilD significantly reduces the ability of S. typhimurium to enter tissue culture cells, whereas a mutation in hilC only modestly affects Salmonella invasion. Based on these results, we have updated our model of Salmonella SPI1 invasion gene regulation. We also speculate on the possible significance of this model for Salmonella pathogenesis.
Mol Microbiol 1999 May
PMID:Two AraC/XylS family members can independently counteract the effect of repressing sequences upstream of the hilA promoter. 1032 May 84


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