Abstract
In some animals, the typical body temperature can be higher than humans, for example, 42°C in poultry and 40°C in rabbits which can be a potential thermal stress challenge for pathogens. Even in animals with lower body temperatures, when infection occurs, the immune system may increase body temperature to reduce the chance of survival for pathogens. However, some pathogens can still easily overcome higher body temperatures and/or rise in body temperatures through expression of stress response mechanisms. Salmonella is the causative agent of one of the most prevalent foodborne illnesses, salmonellosis, and can readily survive over a wide range of temperatures due to the efficient expression of the heat (thermal) stress response. Therefore, thermal resistance mechanisms can provide cross protection against other stresses including the non-specific host defenses found within the human body thus increasing pathogenic potential. Understanding the molecular mechanisms associated with thermal responses in Salmonella is crucial in designing and developing more effective or new treatments for reducing and eliminating infection caused by Salmonella that have survived heat stress. In this review, Salmonella thermal resistance is assessed followed by an overview of the thermal stress responses with a focus on gene regulation by sigma factors, heat shock proteins, along with the corresponding thermosensors and their association with virulence expression including a focus on a potential link between heat resistance and potential for infection.
Highlights
Salmonella is a Gram-negative foodborne pathogen that is a major concern for the food industry and public health authorities because of its capability to cause both widespread contamination and infection within the United States (US) and worldwide [1,2,3,4,5]
DNA replication under heat shock; chaperone protein Prevents aggregation of denatured proteins under hyperosmotic and heat shock Nucleotide exchange factor for DnaK; thermosensor Protease that degrades regulatory proteins Chaperone; maturation of iron–sulfur clusters during heat shock Regulators heat shock response; controls envelope stress response to heat shock, acid stress Thermosensor; temperature-responsive RNA element Unknown but suggested to be a transcriptional regulator Thermosensor endopeptidase; chaperone in the outer membrane and degrades misfolded proteins General stress response sigma factor; DNA repair under stress Involved in intracellular survival of macrophages Outer membrane protein development and assembly; folding of proteins involved in transportation channels Virulence factor regulator under thermal changes aThose involved in both heat shock and virulence
Salmonella spp. have developed thermal resistance mechanisms to overcome these changes in host temperature through the induction of stress response mechanisms
Summary
Salmonella is a Gram-negative foodborne pathogen that is a major concern for the food industry and public health authorities because of its capability to cause both widespread contamination and infection within the United States (US) and worldwide [1,2,3,4,5]. O’Bryan et al [12] reviewed the thermal resistance of Salmonella species and other foodborne pathogens associated with meat and poultry They concluded that a variety of factors and parameters are involved in the thermal resistance and inactivation of those pathogens and spoilage microorganisms such as various temperature exposures, growth phase, and the intrinsic conditions of the food product. When temperature decreases or increases to harmful levels, stress responses (cold and heat shock) are needed to protect the bacterial cell and are thoroughly dependent on bacterial signal transduction mechanisms [24] Genes involved in these mechanisms are regulated at different genetic stages beginning from transcription through translation and into posttranslational levels [25, 26]. Induction of HSP formation is accomplished through the production of chaperones, proteases, and small heat
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