Detection of carcinogens as mutagens in the Salmonella/microsome test: assay of 300 chemicals.
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About 300 carcinogens and non-carcinogens of a wide variety of chemical types have been tested for mutagenicity in the simple Salmonella/microsome test. The test uses bacteria as sensitive indicators for DNA damage, and mammalian liver extracts for metabolic conversion of carcinogens to their active mutagenic forms. Quantitative mutagenicity data from linear dose-response curves are presented: potency varies over a 10(6)-fold range. There is a high correlation between carcinogenicity and mutagenicity: 90% (156/174) of carcinogens are mutagenic in the test and despite the severe limitations inherent in defining non-carcinogenicity, few "non-carcinogens" show any degree of mutagenicity. The results also demonstrate the great utility, and define the limitations, of the test in detecting environmental carcinogens. (+info)
Two murine monoclonal antibodies against serogroup E Salmonellae.
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A monoclonal antibody (MAb), MO15, was raised against the lipopolysaccharide antigen of an epsilon15-lysogenized serogroup E(1) Salmonella strain. The O factor 15-specific MAb MO15, together with another serogroup E-specific MAb, can differentiate among phage lysogenization variants in serogroup E salmonellae. Their epitope specificities in relation to conventional O-antigenic structures are discussed. (+info)
OmpR regulates the two-component system SsrA-ssrB in Salmonella pathogenicity island 2.
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Salmonella pathogenicity island 2 (SPI-2) encodes a putative, two-component regulatory system, SsrA-SsrB, which regulates a type III secretion system needed for replication inside macrophages and systemic infection in mice. The sensor and regulator homologs, ssrAB (spiR), and genes within the secretion system, including the structural gene ssaH, are transcribed after Salmonella enters host cells. We have studied the transcriptional regulation of ssrAB and the secretion system by using gfp fusions to the ssrA and ssaH promoters. We found that early transcription of ssrA, after entry into macrophages, is most efficient in the presence of OmpR. An ompR mutant strain does not exhibit replication within cultured macrophages. Furthermore, footprint analysis shows that purified OmpR protein binds directly to the ssrA promoter region. We also show that minimal medium, pH 4.5, induces SPI-2 gene expression in wild-type but not ompR mutant strains. We conclude that the type III secretion system of SPI-2 is regulated by OmpR, which activates expression of ssrA soon after Salmonella enters the macrophage. (+info)
Salmonellosis in songbirds in the Canadian Atlantic provinces during winter-summer 1997-98.
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From winter 1997 to summer 1998, an epizootic of salmonellosis affected several species of songbirds over a large area of the eastern North American continent. This article describes the details of this epizootic in the Canadian Atlantic provinces, based on laboratory examination of dead affected birds and on suspected but unconfirmed cases of salmonellosis reported by members of the public. The common redpoll (Carduelis flammea) was the species most often affected, followed by pine siskins (C. pinus), purple finches (Carpodacus purpureus), evening grosbeaks (Coccothraustes vespertinus), and American goldfinches (Carduelis tristis). A poor body condition and necrotizing and fibrinopurulent esophagitis and ingluvitis were the most common gross lesions in these birds. Thirty-four of 35 isolates of Salmonella recovered from these birds were identified as phage type 40. Despite the magnitude of this and previous epizootics of salmonellosis among North American songbirds, the sources of these epizootics and the precise influence of environmental factors on their occurrence remain poorly understood. (+info)
Promoter analysis of the class 2 flagellar operons of Salmonella.
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The Salmonella flagellar operons are divided into three classes with reference to their relative positions in the transcriptional hierarchy. Expression of the class 2 operons requires the class 1 gene products, FlhD and FlhC, and is enhanced by an unknown mechanism in the presence of the class 3-specific sigma factor, FliA, and in the absence of its cognate anti-sigma factor, FlgM. In this study, the transcriptional start site mapping was performed by primer extension analysis for five class 2 operons, flgA, flgB, flhB, fliE and fliL. In all cases, one or a few major transcriptional start sites were identified. These start signals disappeared in the flhDC-mutant background, and their intensity decreased and increased in the fliA-mutant and flgM-mutant backgrounds, respectively. Therefore, we conclude that the FlhD/FlhC-dependent transcription is responsible for the FliA-dependent enhancement. Sequence comparison revealed that an imperfect inverted repetitious sequence is conserved upstream of the class 2 operons. Truncation of this sequence from the flgB promoter reduced its transcriptional activity to the background level, indicating that this is an essential cis-acting element for transcription of the class 2 operons. (+info)
Molecular typing of multidrug-resistant Salmonella Blockley outbreak isolates from Greece.
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During 1998, a marked increase (35 cases) in human gastroenteritis due to Salmonella Blockley, a serotype rarely isolated from humans in the Western Hemisphere, was noted in Greece. The two dominant multidrug-resistance phenotypes (23 of the 29 isolates studied) were associated with two distinct DNA fingerprints, obtained by pulsed-field gel electrophoresis of genomic DNA. (+info)
Signal transduction: hair brains in bacterial chemotaxis.
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The conserved cytoplasmic domains of bacterial chemotaxis receptors are a fibrous arrangement of alpha-helical coiled coils that look a lot like hair. Such bundles of alpha-helical filaments mediate sensory-motor responses in all prokaryotic cells. How do they work? Very nearly perfectly is probably as good an answer as any. (+info)
Differential bacterial survival, replication, and apoptosis-inducing ability of Salmonella serovars within human and murine macrophages.
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Salmonella serovars are associated with human diseases that range from mild gastroenteritis to host-disseminated enteric fever. Human infections by Salmonella enterica serovar Typhi can lead to typhoid fever, but this serovar does not typically cause disease in mice or other animals. In contrast, S. enterica serovar Typhimurium and S. enterica serovar Enteritidis, which are usually linked to localized gastroenteritis in humans and some animal species, elicit a systemic infection in mice. To better understand these observations, multiple strains of each of several chosen serovars of Salmonella were tested for the ability in the nonopsonized state to enter, survive, and replicate within human macrophage cells (U937 and elutriated primary cells) compared with murine macrophage cells (J774A.1 and primary peritoneal cells); in addition, death of the infected macrophages was monitored. The serovar Typhimurium strains all demonstrated enhanced survival within J774A.1 cells and murine peritoneal macrophages, compared with the significant, almost 100-fold declines in viable counts noted for serovar Typhi strains. Viable counts for serovar Enteritidis either matched the level of serovar Typhi (J774A. 1 macrophages) or were comparable to counts for serovar Typhimurium (murine peritoneal macrophages). Apoptosis was significantly higher in J774A.1 cells infected with serovar Typhimurium strain LT2 compared to serovar Typhi strain Ty2. On the other hand, serovar Typhi survived at a level up to 100-fold higher in elutriated human macrophages and 2- to 3-fold higher in U937 cells compared to the serovar Typhimurium and Enteritidis strains tested. Despite the differential multiplication of serovar Typhi during infection of U937 cells, serovar Typhi caused significantly less apoptosis than infections with serovar Typhimurium. These observations indicate variability in intramacrophage survival and host cytotoxicity among the various serovars and are the first to show differences in the apoptotic response of distinct Salmonella serovars residing in human macrophage cells. These studies suggest that nonopsonized serovar Typhimurium enters, multiplies within, and causes considerable, acute death of macrophages, leading to a highly virulent infection in mice (resulting in death within 14 days). In striking contrast, nonopsonized serovar Typhi survives silently and chronically within human macrophages, causing little cell death, which allows for intrahost dissemination and typhoid fever (low host mortality). The type of disease associated with any particular serovar of Salmonella is linked to the ability of that serovar both to persist within and to elicit damage in a specific host's macrophage cells. (+info)