دانلود رایگان مقاله انگلیسی پدیداری و پایداری مقاومت فشار بالا در پاتوژن های غذایی مختلف به همراه ترجمه فارسی
| عنوان فارسی مقاله: | پدیداری و پایداری مقاومت فشار بالا در پاتوژن های غذایی مختلف |
| عنوان انگلیسی مقاله: | Emergence and Stability of High-Pressure Resistance in Different Food-Borne Pathogens |
| رشته های مرتبط: | مهندسی صنایع غذایی، علوم مواد غذایی، فناوری مواد غذایی، زیست فناوری مواد غذایی، میکروب شناسی مواد غذایی |
| فرمت مقالات رایگان | مقالات انگلیسی و ترجمه های فارسی رایگان با فرمت PDF میباشند |
| کیفیت ترجمه | کیفیت ترجمه این مقاله خوب میباشد |
| توضیحات | ترجمه این مقاله به صورت خلاصه انجام شده است. |
| نشریه | Asm |
| کد محصول | f269 |
|
مقاله انگلیسی رایگان (PDF) |
دانلود رایگان مقاله انگلیسی |
|
ترجمه فارسی رایگان (PDF) |
دانلود رایگان ترجمه مقاله |
|
خرید ترجمه با فرمت ورد |
خرید ترجمه مقاله با فرمت ورد |
| جستجوی ترجمه مقالات | جستجوی ترجمه مقالات صنایع غذایی |
|
بخشی از ترجمه فارسی مقاله: مقدمه |
|
بخشی از مقاله انگلیسی: High hydrostatic pressure (HHP) processing is currently considered as one of themost promising nonthermalfood preservation techniques and is being used for the commercial pasteurization of an increasing number of food products (7, 18). Typically, pressures in the range of 200 to 600 MPa are applied to inactivate food-borne pathogens and spoilage microorganisms, in order to enhance the safety and extend the shelf life of the product (5, 10, 17, 27). Since this process can be conducted at ambient temperature or in refrigerated conditions, products generally incur less deterioration of nutritional value, flavor, color, and texture than occurs with heating (19). A sustained further exploitation of HHP technology in the food industry, however, requires a more profound understanding of the impact of pressure on microorganisms. In this context, for reasons still not understood, it appears that the susceptibility of vegetative bacteria to HHP varies significantly among different genera and species (2, 28), and even within species as well (4, 23, 31). Indeed, when exposure is to an identical HHP treatment (345 MPa, 5 min, 25°C), the difference in inactivation among different strains of Listeria monocytogenes or Escherichia coli O157:H7 can amount up to 3.5 and 5.6 log cycles, respectively (2). Moreover, studies with E. coli and L. monocytogenes have further revealed that HHP resistance seems to be a trait that can be readily acquired (9, 13, 34). As such, Karatzas et al. (13–15) obtained HHP-resistant mutants of L. monocytogenes Scott A from the small fraction of cells surviving a single HHP shock of 400 MPa (20 min). These spontaneous mutants were typically impaired in the CtsR regulator, which represses type 3 heat shock proteins, and de novo introduction of a ctsR-null allele correspondingly imposed HHP resistance on L. monocytogenes. Interestingly, because of a short but unstable tandem repeat tract in the ctsR gene, it was shown that ctsR mutants actually constituted a preexisting subpopulation in stationary-phase cultures of L. monocytogenes originating from a wild-type inoculum, which explained their isolation already after a single HHP shock (14, 15). In contrast, our group demonstrated the isolation of extremely HHP-resistant mutants of E. coli MG1655 (up to 2 GPa) during a selective enrichment approach based on consecutive cycles of increasingly severe HHP shocks with intermittent resuscitation and outgrowth of the surviving population (9, 34). While their level of HHP resistance by far exceeds that of the L. monocytogenes ctsR mutants, these E. coli MG1655 mutants similarly displayed derepression of a number of heat shock genes (1). Unfortunately, the genetic basis of this extreme HHP resistance in E. coli still remains elusive, although it can reasonably be anticipated that a number of different mutations are required and that the corresponding mutants concomitantly do not naturally preexist in a wild-type population of E. coli MG1655. Spurred by the apparent potential of E. coli MG1655 to develop extreme HHP resistance, and by the importance of this phenomenon for the efficacy and safety of HHP processing, we investigated how readily this trait could evolve in food-related pathogens and how stably it would be maintained in the absence of HHP exposure. MATERIALS AND METHODS Bacterial strains and growth conditions. The different bacteria used in this work are listed in Table 1. E. coli 536 was kindly provided by Erick Denamur (Inserm U722, Paris, France), while the E. coli MG1655A7 mutant as well as its corresponding parental strain (i.e., E. coli MG21) was kindly provided by Nathalie Questembert-Balaban (Hebrew University, Jerusalem, Israel). Unless stated otherwise, stationary-phase cultures were obtained by aerobic growth with shaking (200 rpm) for 23 h in tryptone soy broth (TSB) (Oxoid, Basingstoke, United Kingdom) at 30°C (Pseudomonas aeruginosa, Aeromonas hydrophila, Yersinia enterocolitica, and Listeria innocua) or at 37°C (E. coli, Salmonella enterica serovars Typhimurium and Enteritidis, and Shigella flexneri).When necessary, a final concentration of 100 g/ml ampicillin (Ap100; Applichem, Darmstadt, Germany) was used to select for the presence of pAA212 (encoding the promoter of the dnaK heat shock gene upstream of the green fluorescent protein gene [gfp]; i.e., PdnaK-gfp reporter) (Table 1). During serial passaging (in the absence of HHP treatment), stationary-phase cultures were repeatedly diluted 1/10,000 in prewarmed TSB and grown overnight (24 h) to stationary phase again, until successive growth for ca. 80 generations was achieved (i.e., 6 growth cycles). |